If the design of the flagellum is too complex to have occurred naturally and had to be created by an intelligent creator, does that mean the designer - who posses the intelligence to create the flagellum - was created. Who designed the designer? Or did an intelligent creator pop in to existence in one instant? Does that make more sense than stuff just happening to happen over an extremely long period of time?
@esraretin Because the bacterium with better flagellum were able to out compete those that didn't, the ones that had worse flagellum died and couldn't reproduce. :3
@SorryStamin its not sufficient. there is millions of worse bacteria than flagellums possible ancestors.and they must have been lived for really long time according to possibility in math to produce a great machine like flagellums have.and we are not talkin about one ancestor we are talkin about 50 ancestors so where is even one of them? or wht situation could eliminate them ? so many questions this vid doesnt answer them properly
(cont.) @esraretin sorry, I missed your first comment. Life existed for 2 billion years. As I stated in my first comment evolution of certain traits that help tremendously and are such huge game changers (such as the eye) can evolve quickly as it helps it survive tremendously. What could eliminate them is the ones with better flagellum being able to go to place that are less overcrowded and catch up to ones with worse flagellum and consume them. They are extinct and it is rare to find fossils of
@esraretin But that's exactly how it works, when random things are put in a competing environment the better characteristics always are more if not the only thing abundant! In fact we're all the product of random mutations, you're not a half daddy mommy, you do have mutations along with you, everyone does but most are neutral but once in a while they grow a bit bigger or have a better back for walking. And if you didn't know this goes along even faster in bacteria due to
@SorryStamin yes bacteria propagate faster then we could see lots of complex organs.
e.g can u give an example of most recent species evolved from bacteria,i mean a species that has another complex organ like flagellum or more developed creature evolved most recently from bacteria? or can u give an example of a species which is between single cellular organisms or colonies and multicelular organisms?
@esraretin Although most of those died out as they are inferior there are a couple of species: The most obvious is the underwater sponge mimicking, the first breathing, and animal like creatures. Another fascinating one are the three species of Loricifera, read up on them. I rarely look into bacteria studies, but why would it need to evolve more organelles? It could just improve on the ones it already has as it has all the needs, some might say they got stuck on a peak and the only way to go....
@esraretin I gave you an example. The sea sponge is an early form of animal, yet it is really a colony of cells. I told you about the Loricifera. I will give you a link to know animal transitions. We have jellyfish, brainless masses that can swim. Ediacara biota. All being swept under the rug when the ice sheet melted and caused the Cambrian explosion.
@esraretin petried 1. To convert (wood or other organic matter) into a stony replica by petrifaction. 2. To cause to become stiff or stonelike; deaden. <--- there ya go. I wish you would have told me you were not a first english speaker, I would be happy to continue this conversation over messaging with my google translated text.
@SorryStamin i have a,b,c,d as a main set.results can occur in 4^4 (let assume) way.(as far as i read ,non-synonymous results are more than synonymous ones.then think about for a unique result,limit of result goes to 4^4).Add this ;bcdabdcabdcbabcdbabcdbabcdbacbdabcdabcd (millions of them) to ancesstor DNA Then scientists say somewhere in this sentence,just two letters change and we can think about God. .now probability ignores that letters.we should still think about abababababa>>
@SorryStamin babdbabbdbacdccacad result.then we should calculate the synonymous sentences then probability of uniqe result or synonymous results.i dont think we could even find a few synonymous sentences.my view for my current info level is that its tremendously low probability.even with natural selection because we hadnt to think about god ,we just had to live just like all other animals.
@esraretin Hold on there. If you're talking about knowing when we split up with Chimps, we find genes between us that are different and count the letters that are different. We then estimate the rate of evolution which is surprisingly accurate.
@SorryStamin ''Given the short time since the human-chimpanzee split, it is likely that a few mutations of large effect are responsible for part of the current physical (phenotypic) differences that separate humans from chimpanzees and other great apes''
@esraretin (cont.) higher is down and it would be extremely hard to do that. An example would be the ranging eye systems, could you afford to evolve worse eyes to get new ones? Your species would probably perish.
@esraretin Realize that evolution can both happen slowly and fast, and that it is probable that it could have evolved very quickly, thus reducing the amount of competitors. In comparison the eyes can develop in a minimum of 250,000 generations. And we actually do have a major competing way of getting around, the cilia. And remember these things are probably taking place a billion years ago so any things that were not able to compete would have definitely died out by now.
"...and that it is probable that it [the bacterial flagellum] could have evolved very quickly..."
Not really, considering that it's really implausible for something like the flagellum to evolve through unintelligent co-option. E.g., in this video an ATP synthhase is associated with the passive pore, presumably allowing active transport. But this doesn't work 'cause the ATP synthase would clog up the pore: proteins couldn't pass through a proton transporter (ATP syn.).
@Genomiques Correct me if I'm wrong but isn't ATP synthase a energy slider? Because I think I remember hearing it from somewhere and if that's the case it wouldn't interfere.
ATP synthase transports protons, creating a proton gradient. F0 ATP-synthase, the top part of the ATPase complex, is way too small to allow proteins to be transported through it. That's why flagella lack any homologs at all to the top ATPase proteins. So this step would be likely to clog up the pore, instead of providing an advantage.
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Even if there have only been 10^40 bacteria in history, that is a massive amount. Mutations are relatively common and although most die from these mutations, some would be beneficial and survive. One organism with a beneficial mutation can be the progenitor for a massive chunk of past bacteria, evolution really isn't as mind boggling as you seem to think.
Not when you factor in mutation rates and genome sizes, protein sequence space, etc. I get the feeling you're the one arguing from personal incredulity ("there have been so much bacteria, of course flagella evolved without design!"), while you ignore the actual workings of molecular evolution. If a given biological feature could only evolve through the occurrence of several individually neutral alleles, it's not that likely.
@Genomiques I am actually quite well read on the subject. As the video suggests, the vast majority or the proteins involved have homologues within the cell which means that minimal mutation could result in a flagellum. I'm quite interested in what your background is considering this is generally accepted. When Behe presented this, he was laughed out of court because these things were already understood.
"As the video suggests, the vast majority of the proteins involved have homologues within the cells which means that minimal mutation could result in a flagellum."
Yea, and here's where you're wrong. Watch my video I uploaded just today on the flagellum and homology:
"I'm quite interested in what your background is considering this is generally accepted."
What is generally accepted? Incidentally, even supposing that all flagellar components had meaningful homologies, there are still extensive problems with the idea that "minimal mutation could result in a flagellum." For starters, when the ATP synthase is invoked, this would clog up the passive pore, and be detrimental. That's why flagella lack the upper proteins in their synthases.
@Genomiques "when the ATP synthase is invoked, this would clog up the passive pore, and be detrimental. That's why flagella lack the upper proteins in their synthases." Perhaps you're confused as to what mutations are. It's a given that they would change. Mutations don't just make proteins stick together and a flagellum is magically formed. Mutations cause change, that's the point.
You claim to be well read on the subject, and while you might be well read on the literature on the flagellum and evolution, I doubt you're that well-read in the field of molecular evolution in general. Just saying. Oh, and while I don't deny that many flagellar components share homology with non-flagellar components, this isn't the issue. What is needed are significant homologs that pre-date the flagellum. The TTSS, for example, isn't a pre-cursor system.
@Genomiques I'm studying biochemistry, I'm quite comfortable with evolution on a molecular level. From what I understand, you're right the TTSS isn't a precursor system but there is significant similarity suggesting that both could have arisen from an even more ancient protein with previous function. It is important to point out that, if we couldn't come up with a way the flagellum could have evolved, it doesn't necessarily mean it didn't. There is reason to think that it did however
Actually, the bulk of the evidence suggests that the TTSS evolved directly from the flagellar export system. Gophna et al. is a dissenting view, but their arguments are easily refuted and anyways, as I stated, the evidence certainly points in the direction of the hypothesis that the TTSS evolved directly from the flagellum - the two systems are not monophyletic in other words... (continued)...
...and so any homology between flagellar components and TTSS components do not provide evidence of the co-option of the flagellum.
"There is reason to think it did however..."
Yea, but the reasons aren't very convincing. When you BLAST the flagellar proteins, about a fourth of the flagellar proteins don't have any homologs any where at all, and the significance of the remainder are questionable.
@Genomiques The number of proteins without homologies is even more than 25% but only two of these are considered indispensable. It would not be surprising however if these proteins were the descendants of earlier proteins used for very basic movement or possibly something completely different. The indefensible ones if you're interested are FlgD and FliE, if these 2 proteins had a previous purpose, all of the parts would have been available.
"The number of proteins without homologies is even more than 25% but only two of these are considered indispensable."
Yes, I know, but even though many proteins are not indispensable in flagella, we must nevertheless explain the origin of the entire flagellar structure. I.e., even though Caulobacter flagella seem to be reduced, we must still account for the origin of the Salmonella flagellum, indispensability being irrelevant.
"The indispensable ones you're interested are FlgD and FliE..."
Yea but I'm not interested in indispensable parts. If the origin of the bacterial flagellum is to be explained, we must account for all parts, their indispensability of lack thereof being irrelevant. Thus, about half of the Salmonella flagellum lacks any meaningful homologies. The significance of the other homologies is questionable.
Anyways, I'm offline for the next day, so I'll respond to you then. Take care, and it's always nice to discuss biological origins with someone who can understand the biology behind it ; )
@Genomiques I agree. It goes without saying that much of this is speculation and at some level at least, always will be. What studies such as these provide is possibilities. Once possibilities are available, a designer is not a necessity. Still a possibility, but by no means required. My only objection to people like those at the discovery institute is that they don't seek evidence for their hypothesis, they try to poke holes in others and claim victory. That's not science.
@richjammcl I'm all for people using their resources to attempt refuting theory but only if they're intellectually honest. Saying "we can't figure out how this could have happened through your theory therefore our theory is correct" is a travesty, taking the next step to lobby to misinform others is just wrong. If the science is supported, I'm all for it.
I'm not meaning to boast here, but I am trying to approach the discussion of biological origins with as much intellectual honesty and objectivity as possible. Simply because Darwinian evolution doesn't explain the origin of the flagellum doesn't suddenly mean it was designed. That's "god of the gap" thinking. But hallmarks of intelligent design, such as rational design, as present in the flagellum, and this is positive evidence in favor of a teleological origin.
@Genomiques The reason I pointed out the indispensablity is that, if these parts are accounted for, a flagellum could function allowing for the variety of other proteins to develop over a much longer period of time making it more of a possibility. I have nothing against there being an intelligence or anything like it behind evolutionary processes, I just haven't come across a reason to think that there is. The closest thing to an argument that I've heard is "we aren't sure how this
@richjammcl arose yet so maybe there is something else out there" it's never, here is a reason to think that it's the case. Our understanding of biological processes is far from 100%, it is still developing (I've read some papers suggesting that in some situations mutation resembling Lamarkian ideas may occur). I would agree that it is amazingly complex and difficult to understand, I just don't see a reason YET to think there is any goal behind the processes.
I think that perhaps your problem with seeing teleology behind parts of life is that you're looking for overwhelming evidence. Why not look for clues instead? Certainly, the problem that the flagellum could not have plausibly arisen through purely non-teleological processes, coupled with its rational design, provide an indication that it may have been intelligently designed in some way.
I think that perhaps your problem with seeing teleology behind parts of life is that you're looking for overwhelming evidence. Why not look for clues instead? Certainly, the problem that the flagellum could not have plausibly arisen through purely non-teleological processes, coupled with its rational design, provide an indication that it may have been intelligently designed in some way.
I think that perhaps your problem with seeing teleology behind parts of life is that you're looking for overwhelming evidence. Why not look for clues instead? Certainly, the problem that the flagellum could not have plausibly arisen through purely non-teleological processes, coupled with its rational design, provide an indication that it may have been intelligently designed in some way.
"The reason I pointed out the indispensability is that, if these parts are accounted for, a flagellum could function allowing for the variety of other proteins to develop over a much longer period of time..."
Yea, but since most of the indispensable proteins share no significant sequence similarity with other flagellar proteins, they almost certainly didn't arise through gene duplication...(continued)
(continued from previous comment) ...so this means that even the indispensable proteins would have been co-opted. The problems with cooption as an explanation for the flagellar function are quite real, and furthermore, since these parts are still being co-opted, regardless of their indispensability, we still lack a large amount of any evidence from sequence homology for this cooption.
@Genomiques I'm not suggesting they have sequence similarity to other flagellar proteins, they have sequence similarity to other cellular proteins, that's what homology is so gene duplication is likely. If these proteins are already in the cell, it doesn't take much change for them to operate together, an advantage that would be selected for.
Nor am I. But many of the flagellar proteins in Salmonella (~25%) have absolutely no sequence homologies when one BLASTs them. Thus, they have no sequence homology with other flagellar proteins, which rules out any evidence of flagellar genes being duplicated and then evolving into other flagellar genes, and they also have no sequence homology with other cellular proteins, leaving no evidence of co-option of different proteins.
"If these proteins are already in the cell, it doesn't take much change for them to operate together..."
Uh, you're wrong there. Firstly, any proteins that are co-opted to form a novel molecular machine must have sufficient complementary conformation such that they are able to use energy (e.g., ATP or hydrolysis) to produce a function. There are other problems with the co-option scenario, even graver problems than the simple one above.
@Genomiques I might be misunderstanding the point you're trying to make, are you talking about needing energy to power the flagellum or utilizing energy to associate the proteins? You're undoubtedly aware that there are several domains found in countless proteins that allow them to bind and operate as a unit, diverse proteins having the necessary domains would not be surprising. The proteins performing tasks very similar to their original task but with different results is not
@richjammcl unheard of. These proteins congregating is not that far out, it happens it just typically reduces functionality rather than enhance it. I am not deluded into thinking that any random 40 proteins will form something useful but it is not a stretch to think that co-opting multiple parts to create new function is possible. Like I said, I may have misunderstood your point, but I don't see why it is a problem.
"These proteins congregating is not that far out, it happens it just typically reduces functionality..."
Yes, proteins are able to bind together, but in the vast majority of cases no novel functionality results. Can you cite a single instance in the peer-reviewed literature where a novel protein machine (not cascade system!) has evolved in real-time?
Consider this problem with co-option as an explanation for the origin of the flagellum:
In the above video, you will note that the ATP synthase is associated with the gated, passive pore, forming an active pore. But what if instead the ATP synthase associated with the secretin? No novel functionality would result. And this is true in the vast majority of cases so much so that the co-option is rendered an unsatisfactory explanation for the origin of molecular machines.
@Genomiques I don't see how that is a problem. Maybe such a thing did happen but no novel function resulted, this would not be chosen for. It is important to think big picture, when you have a massive number of organisms all capable of this, many would be useless or even detrimental, not surprisingly, they would not be selected for. All it takes is one to work properly and be selected for. As for citing an instance where this happened, I don't know of one. It takes a massive amount
@richjammcl of time for such a system to develop, individual proteins doing this might not be noticed after all we aren't watching every cell all of the time and it wouldn't be expected to happen regularly or on a large scale. What we have instead is instances it may have happened in the past, for example I could site the bacterial flagellum, it just hasn't been proven because it's amazingly difficult to do.
"It takes a massive amount of time for such a system to develop, individual proteins doing this might not be noticed..."
Well, we've seen the real-time evolution of the PCP degradation pathway, and of nylonase, which refutes the "not watching every cell" argument. These systems are not molecular machines however; they are cascade systems. Why haven't we seen any instances of a two-part protein machine evolving? An interesting question, is it not?
@Genomiques It boggles the mind that you keep using the argument that there haven't been enough. You realize that this could have happened in a small population if everything played out perfectly right? Of course these things don't play out perfectly but that's why large populations make it more likely. The "not watching every cell argument" has not been refuted, just because we've witnessed one does not mean we've witnessed all. We have been witness to an amazingly small portion of life.
"It boggles the mind that you keep using the argument that there haven't been enough."
That's because there haven't been enough. Do the calculations, instead of appealing to your incredulity (i.e., "it boggles the mind" is a sign of personal incredulity, instead of an actual biological argument).
"You realize that this could have happened in a small population if everything played out perfectly right?"
Yea, and I suppose that if everything played out perfectly right then someone could win a series of poker games by every time luckily getting a royal flush. The problem is that things don't work out perfectly, and that's just not how nature works. You're appealing to your own incredulity. Let's be realistic here, instead of fanciful "perfect" hypotheticals.
Consider that for a bacteria species that has only 500 different protein systems, there are 10^150 different possible two-protein system combinations (2^500). Of these different possible systems, how many will not result in any new function? If 10^50 of these combinations did result in novel, beneficial function, there are still 10^100 different non-beneficial systems that must be explored before hitting on just one beneficial one. Not enough bacteria for that.
@Genomiques I think you're misunderstanding probabilities. There is a 1/2 chance that a coin flip will land heads. There is a 1/1032 that I will get 10 heads in a row. That means that I need to flip 1032 times before it becomes likely that I will at some point in the sequence get 10 heads in a row. It is however, possible that the first 10 flips will be heads. In fact, in this case, the first 10 flips being heads is just as likely as any other sequence.
@Genomiques That's irrelevant. There could be 10^99999999999 combinations and that doesn't mean that two proteins that are beneficial couldn't combine in the very first cell. It takes a large number of cells before these particular combinations become LIKELY but they are still very possible. As I pointed out, I need to flip 1032 times before the outcome becomes LIKELY but it could happen in the first 10 flips. Does that much make sense?
Yea, and by that logic all 42 protein components in the flagellum could have been co-opted all at once. There's a reason why Matzke et al. propose step-wise models instead of arguing that the flagellum arose by quantum co-option. Do I really need to start citing peer-reviewed papers that refute your attempt at statistics?
@Genomiques The reason stepwise is assumed is because it is more likely, it relies on a series on unlikely events rather than one massively unlikely event. It's not a difficult concept.
"The reason stepwise is assumed is because it is more likely..."
Actually, the reason step-wise cooption is invoked is because the alternative, quantum co-option, is so unlikely as to be *biologically implausible and unrealistic.* That's why evolutionary biologists like H. Allen Orr repudiate quantum cooption as a general solution to the origin of molecular machines.
@Genomiques How interesting, are you suggesting that they reject one because it is implausible and accept the other in spite the fact that it is also implausible or is it more likely that they think it is plausible?
@Genomiques Likelihood can refer to the unlikely. The papers I am referring to suggest that bacteria can actually induce mutation when it is beneficial to do so. I hasn't been well studied and is still somewhat on the outskirts of biology because it hasn't been proven. I don't know whether or not it actually happens, but it goes to show that we do not have a full picture when it comes to what causes mutations and how common they are.
Please cite the papers. Are you suggesting that bacteria may be able to induce specific mutations at specific sites in their genomes? Is that what you're saying?
@Genomiques Unfortunately I don't have much on hand to reference but here are 2 that might be worth a look if you haven't heard of this before. Nature 335, 142 - 145 (08 September 1988); doi:10.1038/335142a0 and Science 8 June 2001: Vol. 292 no. 5523 pp. 1824-1827 DOI: 10.1126/science.292.5523.1824. As I pointed out, it is not well understood but leaves some interesting possibilities to be explored.
So are you suggesting that bacteria may be able to induce specific mutations to specific genomic sites, thus possibly being an explanation for the origin of molecular machines?
@Genomiques I don't know. I'm simply saying that to assume that these things couldn't have happened because our current understanding has difficulty explaining it does not mean it didn't happen. It would be foolhardy indeed to assume we know every aspect of how these processes occur. As I said before, the only explanation for intelligence I have heard is that we don't currently understand. It's a horrible argument.
"I'm simply saying that to assume that these things couldn't have happened because our current understanding....it does not mean it didn't happen."
Firstly, the suggestion that bacteria may be able to induce specific mutations to specific genomic sites as an explanation for the origin of molecular machines is a *teleological explanation,* (i.e., it's not *random* mutation any more; it's *directed* mutation, which is purely teleological). I have no problem with that.
"...the only explanation for intelligence I have heard is that we don't currently understand. It's a horrible argument."
And an argument I'm not making. I am arguing that molecular machines, like flagella, by virtue of the facts that (a) there are no plausible non-telic explanations for their origin, and (b) their rational design make me very suspicious that teleology may have been behind their origin in some way.
You seem to be saying that we simply don't know really how these molecular machines arose. But if that is what you are saying, then the co-option explanation is not the default explanation, and a teleological explanation should be opposed no more than a non-teleological explanation, unless one is more robust. The rational design inherent to the core flagellar structure is positive evidence in favor of the telic view.
@Genomiques (a) Again, there may not be any plausible non-telic explanations that we know of but that doesn't mean there aren't any, that's not an argument. (b) Appearance of design does not necessarily suggest design. Looking at the beautiful lattice of salt crystals might suggest they were crafted by little artists but there is no reason to think that they are not governed by the same principles that create any other crystals.
@richjammcl As I've pointed out, I wouldn't rule out design, it is possible. In terms of which hypothesis is more robust; One relies on natural forces and processes at least some of which are known and many are well understood. The other relies on a prime mover and again, saying this thing looks like something that one might design is not the same as saying this could not have not been designed. We have no evidence for this designer apart from the appearance of design which we don't
@richjammcl even know is or is not designed yet. Given that we can't realistically tell the difference, I fail to see how appearance of design could ever be considered evidence.
I'm not even arguing from appearance of design. Whatever gave you that idea? The telic hypothesis is just as robust as the non-telic hypothesis. You might want to look into the front-loading hypothesis, an inherently telic hypothesis, and it is very testable.
@Genomiques An interesting theory, are you suggesting panspermia then? It certainly seemed like you were toting the importance of appearance of design. It might be helpful to point out how you could possibly discern between something that was "rationally designed" and something that was not rationally designed but has purpose.
Not meaning to be pedantic, but you mean *hypothesis.* Front-loading is a bit like panspermia, I suppose, but I think panspermia doesn't necessarily entail teleology. Panspermia, as I understand it, simply posits that the first life forms on earth came from outer space. The front-loading hypothesis goes one more step ahead from this, and suggests that earth was seeded with life that had the genes to shape subsequent evolution.
"In terms of which hypothesis is more robust...one relies on natural forces..."
Uh, teleology also relies on natural laws. You yourself acknowledged, implicitly at least, that bacteria may be able to induce specific mutations at specific genomic sites, thereby being able to explain the origin of molecular machines. This is a purely teleological explanation, and your problem with this telic explanation is?
@Genomiques Perhaps we mean different things when we talk about design. I'm not sure if you looked at the papers I referenced but they don't suggest that bacteria decide that x is beneficial so I'm going to mutate to do that. There may be processes at play which, when confronted with death, bacteria induce mutations at a greater rate increasing the likelihood that one in a colony will have the required mutation and will then repopulate the colony, the rest of whom will be dead.
"There may be processes at play which, when confronted with death, bacteria induce mutations at a greater rate..."
Oh, well, if that's one of your solutions to the origin of molecular machines then it's not at all that great. Simply accelerating the mutation rate doesn't offer a solution to the origin of molecular machines if these mutations are specified.
@Genomiques One of your issues is that there hasn't been enough bacteria for this to occur, massively increasing mutation rate means that there are considerably less bacteria needed before this becomes likely. And again, something does not have to be extremely likely to happen, only plausible.
"One of your issues is that there hasn't been enough bacteria for this to occur, massively increasing mutation rate means that there considerably less bacteria needed..."
Yea but there is a maximum possible mutation rate before mutation rates become lethal. The mutation rates of viruses are near the maximum mutation rate, so you can't get any "faster" than the mutation rate that becomes lethal. I'll try to get the PNAS paper on that: can't think of what the title was.
@Genomiques Of course if you let mutation run free you will inevitably destroy your genome and die. However, on a large scale, increasing mutation rate means a large number of mutations without any one organism reaching particularly high mutation rates. Many, if not most of the organisms involved would not receive anything useful and might even die but on occasion, you will receive the mutation you need. Putting a colony of bacteria on a medium rich in antibiotic shows how,
@richjammcl while most organisms will die, some will have a beneficial mutation and survive. They quickly reproduce and, to an untrained eye, it appears that the bacteria were unaffected by the antibiotic. Of course that's not the case, just a massive amount of dead bacteria were replaced with new, more fit bacteria. All it takes is one bacteria to receive a beneficial mutation and it can outperform its brethren.
For example, if an ATP synthase can, via a mutation, associate with a passive pore, there is nothing stopping it from associating with another ATP synthase, a secretin, an ion channel, an adhesive protein, etc. In other words, the ratio of mutations that will result in a novel molecular machine versus those that will not result in beneficial function is far different than the case with antibiotics.
@Genomiques That's fair, but if it has the ability to associate with all of these things and one is useful, this organism will be selected for. Granted, much of its progeny will have a minimal advantage, but an advantage none the less. From that point, specificity can be developed. Keeping in mind that, while the whole motor wouldn't appear over night in one organism, it is possible that multiple steps were in development at the same time, yet another way that the minimal amount of
@richjammcl bacteria and time is less. On top of these things, organisms have systems in place to minimize mutation rates because it is so often detrimental but if we're looking at bacteria before basic motility was achieved, we're going back in time to a point where its ability to correct mutation would have been less efficient. Mutation would have been more common and accelerating these pathways is hypothetically possible.
"...but if we're looking at bacteria before basic motility was achieved, we're going back in time to a point where its ability to correct mutation would have been less efficient."
This is circular reasoning in its most blatant form. Because you have non-teleological filters on, you're assuming that the proof-reading machinery of the cell had to evolve its efficiency. Thus, you're making an assumption that proof-reading machinery was less efficient in the past.
@Genomiques And you're assuming that it didn't. If this wasn't an assumption you're making you wouldn't be able to say there haven't been enough bacteria in existence because we would know little about how often mutations occurred in early life.
You rely way too much on bacteria population sizes and mutation rates. But if a cell has only 500 different protein systems, how many 2 protein combinations are possible? A total of 10^150. Of these, the vast majority will be non-beneficial combinations. Even being extremely generous and assuming 10^50 will be beneficial, that still leaves 10^100 combinations to be explored before it's likely a single beneficial system will arise.
@Genomiques Of course I rely on population sizes, they're a necessity. For example, it is incredibly unlikely that if I buy a lottery ticket that I'll have the winning numbers. That doesn't mean that no one wins the lottery, it happens regularly. Granted we're talking about statistics many orders of magnitude larger but we're also dealing with populations many orders of magnitude larger.
You forget that there are far, far more possible two-protein combinations that will not be beneficial than there are combinations that will be beneficial. If any ATP synthase can associate with those proteins, nothing is stopping those proteins from ALSO associating with each other, with no beneficial result.
@Genomiques Given that many of these proteins existed pre-flagellum, it is possible that the mutation was for specificity and not random binding properties that allowed the protein to interact with anything in it's path.
"Given that many of these proteins existed pre-flagellum, it is possible that the mutation was for specificity and not random binding properties..."
That's not the point. If it can have a specific mutation that allows it to bind with one protein, there's nothing stopping it from having mutations that would allow it to bind with other proteins, even though these interactions wouldn't result in novel function.
@Genomiques Of course there's nothing stopping that! As I have said multiple times, there were undoubtedly countless mutations that were useless and countless more that were deadly, the point is that when one that is beneficial occurs, it is selected for and that organisms progeny multiply and go on to have many more useless mutations until one of them has a beneficial mutation and it happens again. There are many losing lottery tickets, you don't hear about the many many people who
"...the point is that when one that is beneficial occurs.."
Right, and what if the ratio of beneficial/non-beneficial protein combinations was 1:10^100. This means that 10^100 combinations will be explored before any one beneficial combination will occur. Not so with the lottery. With the lottery, the ratio of win/no wins might be 1: 1,000,000. So if one million people buy lottery tickets, one will win.
@Genomiques Even if you're ratio of 1:10^100 is correct, and I don't think that it is, you don't have to go through all 10^100 to find the right one. If there are 10 balls in a bag and only one is red and that's the one I need, there is no reason for me to keep looking if the red one is the second ball I pull. This is broken math, 1:10^100 does not mean it will take 10^100 mutations to get the right one.
"1:10^100 does not mean it will take 10^100 mutations to get the right one."
Yes, it does, unless some cell is extraordinarily lucky - and that's appealing to miracle, not to biotic reality. That's why the odds of a given function evolving decreases exponentially the more gene products are required for that function (and assuming no intermediates are functional).
@Genomiques For example, the odds of winning the 6/49 are 1:13,983,816. That means if you play every week, it takes 13,983,816 weeks before you are LIKELY to win the lottery. Some how, people win the lottery on a regular basis however. By the same logic though, they haven't played enough times for this to happen. It's just wrong.
The ratios are different here. Millions of people buy lottery tickets, making the *total ratio* wins/no wins different. The odds of ONE person winning the lottery is 1:13,983,816, but that *someone* in a pool of a million people wining is 1,000,000:13,983,816.
@Genomiques Exactly, hence the large populations of bacteria referred to previously. "Yes, it does, unless some cell is extraordinarily lucky" if you honestly think that you don't understand basic probabilities. There's a 1/6 chance that I'll roll a 4. That doesn't mean that I need to roll 6 times to get a four and it doesn't mean anything remotely strange happened if my first roll was a 4. I'm not saying that the mutation required happened the first time every time, that would
@richjammcl ridiculous but to think it happened the 10^100th time every time is equally ridiculous. It might have happened the first time, the 50 000th time the 10^62 time or the 10^100 time, all of which are equally likely unless there is some process at work to keep it from happening.
I can bring up many instances where probabilities are applied in the way I am applying it, from the peer-reviewed literature. Furthermore, if your logic was correct, then a basic argument for common descent - nested hierarchical patterns that result from protein sequence alignments - falls apart, simply because one could, by your logic, argue that this pattern is merely the result of chance. After all, all patterns are equally likely. You're misunderstanding probability.
@Genomiques Peer review has been wrong before, people often make simple mathematical mistakes. Let's make this very simple, when rolling a dice, is any one number more likely than the others? No. There is a 1/6 chance for each. If I roll a 1, is that strange? No. Any of the other numbers? No. So even though there is a 1/6 chance in rolling any one number, one of the numbers has to be rolled. Therefore one of the numbers came up earlier than you were expecting if you
@richjammcl were expecting it to take six rolls. With protein compatibility, even if it was a 10^100 chance, if one of those mutations happened it obviously did not take 10^100 mutations. If all mutations are equally likely, the beneficial mutation could come up anywhere in that sequence could it not? I fail to see why that is confusing for you.
When I align DUTpase of E. coli and Salmonella, there is ~92% sequence identity. From this I can reasonable conclude that the two sequences share a common ancestor. However, by your logic we could just as reasonably conclude that that sequence identity was the result of chance, true? I wonder why every biologist would disagree with you.
@Genomiques It is hypothetically possible but, as the number of steps increase, the odds decrease. For example, if I rolled a 6 it wouldn't be surprising if my next roll was also a 6. By contrast, if I rolled 43242342134234234235153142342353256 in succession the rolled 43242342134234234235153142342353256 again it would be surprising. It is just as likely as any other individual sequence but there are more different sequences than identical, that's what makes it unlikely.
"It is just as likely as any other individual sequence, but there are more different sequences than identical, that's what makes it unlikely."
Exactly. There are far more non-beneficial combinations than beneficial protein combinations, that's what makes the co-option scenario an unlikely explanation for the origin of molecular machines like flagella.
@Genomiques It feels like we're just spinning in circles now. If you're interested in the probabilities I was trying to explain earlier that you think don't make sense, I'd recommend a book called Innumeracy, it's about common mathematical mistakes we often make. Ultimately I think we're just disagreeing about what we personally consider plausibility. Regardless, there are countless unlikely events that occur every day without anyone forcing them to happen.
@Genomiques What!? You think that once something happens it becomes likely? Flipping a coin 1000 times and getting 1000 heads is unlikely. If I did it, it's something unlikely, happening. It is still unlikely.
Anyways, you really don't seem to be grasping my point. Flagellar evolution is unlikely for the same basic reason that it's unlikely for two unrelated sequences to converge, by chance, into nearly identical sequences.
"I really don't see how those two scenarios are remotely similar."
Then WHY is it unlikely for two unrelated sequences to, by chance, happen to have nearly the same sequence identity? The answer to that question is my answer to your arguments over probability and co-option.
@Genomiques One requires two long identical processes. That is unlikely. One process is comparatively far more likely. Even if we are dealing with very improbable events, it is unlikely to happen but exponentially less likely to happen twice in the same way. There is convergent evolution but that produces two different structures with similar function not two identical structures.
Yes, BUT by your argument, one sequence matching another sequence is just as likely as any other sequence. I'm not talking about convergent evolution here because that would no longer be pure chance: natural selection would be in the equation.
@Genomiques yes, both are equally likely but in the case of two systems, there are more possibilities. For example, rolling a 6, 1/6. Rolling 2 dice and them both be 6, 1/36. The six is just as likely on each die and they don't influence each other but there are more possibilities so it becomes less likely.
"...but there are more possibilities so it becomes less likely."
Yes, AND there are far more possible protein combinations that are not beneficial than there are protein combinations that are beneficial, so the latter is less likely.
@Genomiques Are we seriously going over this again? I have already conceded that a useless of damaging mutation is more likely than a beneficial one. Natural selection is a mechanism by which that doesn't matter. You can have negative mutations all you want, you'll die and that's the end of it. If you have a beneficial mutation you procreate. There have been countless detrimental mutations over the years, those organisms die. That's the idea.
"I have already conceded that a useless or damaging mutation is more likely than a beneficial one."
Yes, and at the level of molecular machines, by even the most generous estimates, non-beneficial mutations are 10^100 more likely than a single mutation that would associate two proteins that would just happen to form a novel function.
Refer back to my estimates. With 500 different protein systems, there are 2^500 = 10^150 different possible two-protein combinations. Of these, the vast majority will be non-beneficial. Even assuming that 10^50 of these protein systems will be beneficial, this still means that for every beneficial protein system, there will be 10^100 non-beneficial systems.
@Genomiques That is assuming that many other potentially useful combinations are not useful because they haven't occurred. Regardless, it completely ignores things such as, proteins that function in proximity are far more likely to interact than proteins that are not, it assumes that all proteins are equally likely to associate which might not be the case. Its not like we're throwing a pile of Lego together and seeing what sticks, not all proteins are created equal.
"That is assuming...because they haven't occurred."
Not at all. Regarding your other points:
a) Proteins that function in proximity are not far more likely to interact *through virtue of mutation.* They may interact with proteins in close proximity, through chemical bonds, etc., but if this association is not genetical than it's not evolutionarily meaningful.
b) Name one reason why proteins would not be equally likely to association with each other.
@Genomiques That is an assumption you're making, there could be countless that just haven't occurred that you're passing off as detrimental. a) If a protein has a mutation that gives it the ability to bond to another protein, it is absolutely more likely to interact with a protein it comes into contact with rather than one it does not come into contact with. b) For exampleif a protein has one spot to dock vs multiple, their docking sites could be more or less available to the outside
a) A protein is just as likely to have a mutation that allows protein-protein binding as it is to have a mutation that localizes it to another subcellular location, thus making it capable of binding with proteins it previously did not interact with.
b) I don't see how this makes protein X more likely to associate with protein Y than with, say protein Z. Elaborate.
@Genomiques a) again, if the protein mutates and does something that is not needed it is not chosen for. b) If protein x has a new binding domain that allows it to interact with either Y or Z but Y has multiple binding sites and Z has one, it has a better chance of binding to Y. It might still bind to Z but with less frequency. Increased specificity will be selected for. Lets say for the sake of argument that binding to Y is beneficial and Z is detrimental. If the benefits are
@richjammcl roughly equal to the detriment but binding to Y happens considerably more often than to Z, this is something that can be selected for. After this point, increased selectivity can be selected for because, naturally, having the benefit alone is better than the benefit and detriment together.
@richjammcl If it can bind to a binding site on both Y and Z but Y has a binding site on the outside and Z has a binding site somewhat blocked by protein structure, it is more likely to bind to Y.
a) This part of your argument is irrelevant to what we're currently discussing: whether a protein is just as likely to bind to one protein as to another.
b) This argument of yours is reasonable, but it doesn't really affect my core argument significantly since in most cases, a random protein will be just as likely to bind to a protein than to another, except in the few cases where a given protein has more binding sites.
@Genomiques a) This is relevant. Although there are a huge number of proteins in any given cell, there are a limited amount that each protein will come into contact with. A protein could mutate in such a way that if it were to bind to any number of proteins it would be catastrophic. If the protein never comes into contact with these proteins and does come into contact with a beneficial one, that damaging mutation is anything but. b) Although that is true, it does
@richjammcl limit the number of proteins that a mutated protein might bind to. Since the argument we are discussing is that there are a massive amount of proteins that a protein could interact with, limiting the number is relevant.
You know what, I think that this discussion can hardly be resolved in the 500 character limit of YouTube, and so I'll put together a video on cooption in the next week or so, where I'll use animations et al. to try to get my point across. If you wish to continue this discussion that's fine, but I think at the moment you might be more interested in discussing this: what biological feature would make *you* suspicious that teleology played a role in the history of life?
@Genomiques Difficult to say really. I don't think it would be any one feature. As I see the argument it is that we don't understand how it happened so maybe there's a designer. Or, I suppose, your variety is somewhat closer to it seems so improbable that I suspect a designer. I think that's the wrong way to go about it personally, seems backwards. I would be interested in seeing how this front loading idea plays out. I'm not sure how it would prove design, but I think it
@richjammcl at least has the massive advantage over most ID claims in that it's testable. That's how real science works, take a claim and try to prove it wrong, see what's left standing at the end of the day instead of throwing our hands up and saying it couldn't have happened that fast in that population because that doesn't make sense to me.
At the moment, I'm not looking for proof of teleology. I'm looking for the clues and the evidences in favor of the front-loading hypothesis. There are several ways to test the front-loading hypothesis, and if it's predictions are confirmed, then it is considerably strengthened. Of course, nowhere in this discussion do we mention any gods. Anyone who assumes the intelligence must be supernatural by any means is clearly not that acquainted with the workings of science.
@Genomiques Yeah, the problem it would have is much the same as abiogenic hypotheses, even if you can make it happen it is still only a possibility. Abiogenesis is an interest of mine and it can be quite frustrating playing in that arena. In regards to your question, I'm not sure there is a feature that would make me suspicious. It's always a possibility in the back of my head because I can't think of a way to disprove it, but never the less, it wouldn't be my go to explanation for
@richjammcl anything. I find the idea of directed panspermia quite interesting and I think we'll very likely pull it off ourselves but I haven't seen anything that would make me think it's any more likely than the other ideas at hand. A bit of Occams razor I suppose, we just see the cut a little differently.
@Genomiques Haha, and to you. I just looked and we've taken up the past 16 pages of comments. Perhaps this conversation would be more appropriate for inbox messages.
I agree. I'll send you a message to your inbox as soon as possible, on front-loading and how we can test it - if you're interested in that. I'll try to do that tomorrow, 'cause right now I'm kinda busy. Have a good evening.
Remember, I'm not necessarily talking about evidence in the sense that it would convince you of that teleology played a role. I'm talking about clues. What kind of clues would make you a bit suspicious? By the way, I do not conclude teleology solely on the basis of a lack of a non-telic explanation. Rather, the lack of a non-telic explanation is just one factor that shifts the balance in favor of the telic hypothesis.
Yea but accelerating the mutation rate still doesn't solve the problem. Even if you increased the mutation rate to every thousandth nucleotide being mutated, the problems with evolving a molecular machine are still very real. Resistance to antibiotics evolve quickly enough because only a few point mutations are needed. With chloroquine resistance in malaria, just one point mutation will be beneficial. Things are different with molecular machines.
"Appearance of design does not necessarily suggest design."
It does *suggest* design, but it is not in itself positive evidence of intelligent design. Rational design, however, is a hallmark of rational minds and thus it is positive evidence in favor of the telic hypothesis. The discontinuity of the flagellum from things known to be able to have evolved, *coupled with its rational design* is at least a clue that teleology might be at play here.
Anything with a probability above 0 is POSSIBLE. It is *possible* that I will win a poker game by getting a string of royal flushes in a row. But *possibility* should not be confused with *plausibility.* Of course, the odds of the flagellum evolve through cooption are above 0, thus it is possible. But it's not biologically *realistic.*
If the design of the flagellum is too complex to have occurred naturally and had to be created by an intelligent creator, does that mean the designer - who posses the intelligence to create the flagellum - was created. Who designed the designer? Or did an intelligent creator pop in to existence in one instant? Does that make more sense than stuff just happening to happen over an extremely long period of time?
LexMassive 4 days ago
@LexMassive I agree with this statement!
SorryStamin 3 days ago
its bullshit then why ancesstors went dinstiction? u have to give the reasons.and this vid doesnt sound like a good explanation.thx to Behe
esraretin 3 weeks ago
@esraretin Because the bacterium with better flagellum were able to out compete those that didn't, the ones that had worse flagellum died and couldn't reproduce. :3
SorryStamin 1 week ago
@SorryStamin its not sufficient. there is millions of worse bacteria than flagellums possible ancestors.and they must have been lived for really long time according to possibility in math to produce a great machine like flagellums have.and we are not talkin about one ancestor we are talkin about 50 ancestors so where is even one of them? or wht situation could eliminate them ? so many questions this vid doesnt answer them properly
esraretin 1 week ago
(cont.) @esraretin sorry, I missed your first comment. Life existed for 2 billion years. As I stated in my first comment evolution of certain traits that help tremendously and are such huge game changers (such as the eye) can evolve quickly as it helps it survive tremendously. What could eliminate them is the ones with better flagellum being able to go to place that are less overcrowded and catch up to ones with worse flagellum and consume them. They are extinct and it is rare to find fossils of
SorryStamin 1 week ago
@SorryStamin i cant believe complex organs can evolve very quickly when i think about random mutations.
esraretin 1 week ago
@esraretin But that's exactly how it works, when random things are put in a competing environment the better characteristics always are more if not the only thing abundant! In fact we're all the product of random mutations, you're not a half daddy mommy, you do have mutations along with you, everyone does but most are neutral but once in a while they grow a bit bigger or have a better back for walking. And if you didn't know this goes along even faster in bacteria due to
SorryStamin 1 week ago
@esraretin (cont.) conjugation and the point they can reproduce rather quickly.
SorryStamin 1 week ago
@SorryStamin yes bacteria propagate faster then we could see lots of complex organs.
e.g can u give an example of most recent species evolved from bacteria,i mean a species that has another complex organ like flagellum or more developed creature evolved most recently from bacteria? or can u give an example of a species which is between single cellular organisms or colonies and multicelular organisms?
esraretin 1 week ago
@esraretin Although most of those died out as they are inferior there are a couple of species: The most obvious is the underwater sponge mimicking, the first breathing, and animal like creatures. Another fascinating one are the three species of Loricifera, read up on them. I rarely look into bacteria studies, but why would it need to evolve more organelles? It could just improve on the ones it already has as it has all the needs, some might say they got stuck on a peak and the only way to go....
SorryStamin 1 week ago
@SorryStamin i see enormous gap in single cellular or colonies to animals or plants
esraretin 1 week ago
@esraretin I gave you an example. The sea sponge is an early form of animal, yet it is really a colony of cells. I told you about the Loricifera. I will give you a link to know animal transitions. We have jellyfish, brainless masses that can swim. Ediacara biota. All being swept under the rug when the ice sheet melted and caused the Cambrian explosion.
SorryStamin 1 week ago
@SorryStamin i searching for some info.im new english learner.could u say what means?
The first vascular plant fossils (dated back to about 400 million years ago) have ''petried'' mycorrhizae. i couldnt find meaning of ''petried''?
esraretin 1 week ago
@esraretin petried 1. To convert (wood or other organic matter) into a stony replica by petrifaction. 2. To cause to become stiff or stonelike; deaden. <--- there ya go. I wish you would have told me you were not a first english speaker, I would be happy to continue this conversation over messaging with my google translated text.
SorryStamin 1 week ago
@SorryStamin i have a,b,c,d as a main set.results can occur in 4^4 (let assume) way.(as far as i read ,non-synonymous results are more than synonymous ones.then think about for a unique result,limit of result goes to 4^4).Add this ;bcdabdcabdcbabcdbabcdbabcdbacbdabcdabcd (millions of them) to ancesstor DNA Then scientists say somewhere in this sentence,just two letters change and we can think about God. .now probability ignores that letters.we should still think about abababababa>>
esraretin 1 week ago
@SorryStamin babdbabbdbacdccacad result.then we should calculate the synonymous sentences then probability of uniqe result or synonymous results.i dont think we could even find a few synonymous sentences.my view for my current info level is that its tremendously low probability.even with natural selection because we hadnt to think about god ,we just had to live just like all other animals.
esraretin 1 week ago
@esraretin Hold on there. If you're talking about knowing when we split up with Chimps, we find genes between us that are different and count the letters that are different. We then estimate the rate of evolution which is surprisingly accurate.
SorryStamin 1 week ago
@esraretin (cont.) algae would be considered a colony right? all it does is stay by other algae.
SorryStamin 1 week ago
@SorryStamin ''Given the short time since the human-chimpanzee split, it is likely that a few mutations of large effect are responsible for part of the current physical (phenotypic) differences that separate humans from chimpanzees and other great apes''
these men have to calculate possibility of it!
esraretin 1 week ago
@esraretin (cont.) higher is down and it would be extremely hard to do that. An example would be the ranging eye systems, could you afford to evolve worse eyes to get new ones? Your species would probably perish.
SorryStamin 1 week ago
@esraretin (cont.) And by bacteria organelles I meant basically better new bacteria. Sorry for any confusion.
SorryStamin 1 week ago
cnot. @esraretin such ancestors.
SorryStamin 1 week ago
@SorryStamin i mean wht could eliminate the strong ancestors ? because they must lived for really long time so they were indeed powerfull species
esraretin 1 week ago
@esraretin Realize that evolution can both happen slowly and fast, and that it is probable that it could have evolved very quickly, thus reducing the amount of competitors. In comparison the eyes can develop in a minimum of 250,000 generations. And we actually do have a major competing way of getting around, the cilia. And remember these things are probably taking place a billion years ago so any things that were not able to compete would have definitely died out by now.
SorryStamin 1 week ago
@SorryStamin
"...and that it is probable that it [the bacterial flagellum] could have evolved very quickly..."
Not really, considering that it's really implausible for something like the flagellum to evolve through unintelligent co-option. E.g., in this video an ATP synthhase is associated with the passive pore, presumably allowing active transport. But this doesn't work 'cause the ATP synthase would clog up the pore: proteins couldn't pass through a proton transporter (ATP syn.).
Genomiques 4 days ago
@Genomiques Correct me if I'm wrong but isn't ATP synthase a energy slider? Because I think I remember hearing it from somewhere and if that's the case it wouldn't interfere.
SorryStamin 3 days ago
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@SorryStamin
What do you mean by "energy slider"? o.o
ATP synthase transports protons, creating a proton gradient. F0 ATP-synthase, the top part of the ATPase complex, is way too small to allow proteins to be transported through it. That's why flagella lack any homologs at all to the top ATPase proteins. So this step would be likely to clog up the pore, instead of providing an advantage.
Genomiques 1 day ago
@esraretin You sound really smart.
Gunner7121 1 week ago in playlist Liked videos
@Gunner7121 sarcasm ? if not thank u
esraretin 1 week ago
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TrumpetCallofGodLT 1 month ago in playlist Evidence FOR Evolution and Against Creationism
Even if there have only been 10^40 bacteria in history, that is a massive amount. Mutations are relatively common and although most die from these mutations, some would be beneficial and survive. One organism with a beneficial mutation can be the progenitor for a massive chunk of past bacteria, evolution really isn't as mind boggling as you seem to think.
richjammcl 1 month ago
@richjammcl
"...that is a massive amount..."
Not when you factor in mutation rates and genome sizes, protein sequence space, etc. I get the feeling you're the one arguing from personal incredulity ("there have been so much bacteria, of course flagella evolved without design!"), while you ignore the actual workings of molecular evolution. If a given biological feature could only evolve through the occurrence of several individually neutral alleles, it's not that likely.
Genomiques 1 month ago
@Genomiques I am actually quite well read on the subject. As the video suggests, the vast majority or the proteins involved have homologues within the cell which means that minimal mutation could result in a flagellum. I'm quite interested in what your background is considering this is generally accepted. When Behe presented this, he was laughed out of court because these things were already understood.
richjammcl 1 month ago
@richjammcl
"As the video suggests, the vast majority of the proteins involved have homologues within the cells which means that minimal mutation could result in a flagellum."
Yea, and here's where you're wrong. Watch my video I uploaded just today on the flagellum and homology:
watch?v=hDki3Wk4A1E&feature=watch_response
Genomiques 1 month ago
@richjammcl
"I'm quite interested in what your background is considering this is generally accepted."
What is generally accepted? Incidentally, even supposing that all flagellar components had meaningful homologies, there are still extensive problems with the idea that "minimal mutation could result in a flagellum." For starters, when the ATP synthase is invoked, this would clog up the passive pore, and be detrimental. That's why flagella lack the upper proteins in their synthases.
Genomiques 1 month ago
@Genomiques "when the ATP synthase is invoked, this would clog up the passive pore, and be detrimental. That's why flagella lack the upper proteins in their synthases." Perhaps you're confused as to what mutations are. It's a given that they would change. Mutations don't just make proteins stick together and a flagellum is magically formed. Mutations cause change, that's the point.
richjammcl 1 month ago
@richjammcl
You claim to be well read on the subject, and while you might be well read on the literature on the flagellum and evolution, I doubt you're that well-read in the field of molecular evolution in general. Just saying. Oh, and while I don't deny that many flagellar components share homology with non-flagellar components, this isn't the issue. What is needed are significant homologs that pre-date the flagellum. The TTSS, for example, isn't a pre-cursor system.
Genomiques 1 month ago
@Genomiques I'm studying biochemistry, I'm quite comfortable with evolution on a molecular level. From what I understand, you're right the TTSS isn't a precursor system but there is significant similarity suggesting that both could have arisen from an even more ancient protein with previous function. It is important to point out that, if we couldn't come up with a way the flagellum could have evolved, it doesn't necessarily mean it didn't. There is reason to think that it did however
richjammcl 1 month ago
@richjammcl
Actually, the bulk of the evidence suggests that the TTSS evolved directly from the flagellar export system. Gophna et al. is a dissenting view, but their arguments are easily refuted and anyways, as I stated, the evidence certainly points in the direction of the hypothesis that the TTSS evolved directly from the flagellum - the two systems are not monophyletic in other words... (continued)...
Genomiques 1 month ago
@richjammcl
...and so any homology between flagellar components and TTSS components do not provide evidence of the co-option of the flagellum.
"There is reason to think it did however..."
Yea, but the reasons aren't very convincing. When you BLAST the flagellar proteins, about a fourth of the flagellar proteins don't have any homologs any where at all, and the significance of the remainder are questionable.
Genomiques 1 month ago
@Genomiques The number of proteins without homologies is even more than 25% but only two of these are considered indispensable. It would not be surprising however if these proteins were the descendants of earlier proteins used for very basic movement or possibly something completely different. The indefensible ones if you're interested are FlgD and FliE, if these 2 proteins had a previous purpose, all of the parts would have been available.
richjammcl 1 month ago
@richjammcl
"The number of proteins without homologies is even more than 25% but only two of these are considered indispensable."
Yes, I know, but even though many proteins are not indispensable in flagella, we must nevertheless explain the origin of the entire flagellar structure. I.e., even though Caulobacter flagella seem to be reduced, we must still account for the origin of the Salmonella flagellum, indispensability being irrelevant.
Genomiques 1 month ago
@richjammcl
"The indispensable ones you're interested are FlgD and FliE..."
Yea but I'm not interested in indispensable parts. If the origin of the bacterial flagellum is to be explained, we must account for all parts, their indispensability of lack thereof being irrelevant. Thus, about half of the Salmonella flagellum lacks any meaningful homologies. The significance of the other homologies is questionable.
Genomiques 1 month ago
@richjammcl
Anyways, I'm offline for the next day, so I'll respond to you then. Take care, and it's always nice to discuss biological origins with someone who can understand the biology behind it ; )
Genomiques 1 month ago
@Genomiques I agree. It goes without saying that much of this is speculation and at some level at least, always will be. What studies such as these provide is possibilities. Once possibilities are available, a designer is not a necessity. Still a possibility, but by no means required. My only objection to people like those at the discovery institute is that they don't seek evidence for their hypothesis, they try to poke holes in others and claim victory. That's not science.
richjammcl 1 month ago
@richjammcl I'm all for people using their resources to attempt refuting theory but only if they're intellectually honest. Saying "we can't figure out how this could have happened through your theory therefore our theory is correct" is a travesty, taking the next step to lobby to misinform others is just wrong. If the science is supported, I'm all for it.
richjammcl 1 month ago
@richjammcl
I'm not meaning to boast here, but I am trying to approach the discussion of biological origins with as much intellectual honesty and objectivity as possible. Simply because Darwinian evolution doesn't explain the origin of the flagellum doesn't suddenly mean it was designed. That's "god of the gap" thinking. But hallmarks of intelligent design, such as rational design, as present in the flagellum, and this is positive evidence in favor of a teleological origin.
Genomiques 1 month ago
@Genomiques The reason I pointed out the indispensablity is that, if these parts are accounted for, a flagellum could function allowing for the variety of other proteins to develop over a much longer period of time making it more of a possibility. I have nothing against there being an intelligence or anything like it behind evolutionary processes, I just haven't come across a reason to think that there is. The closest thing to an argument that I've heard is "we aren't sure how this
richjammcl 1 month ago
@richjammcl arose yet so maybe there is something else out there" it's never, here is a reason to think that it's the case. Our understanding of biological processes is far from 100%, it is still developing (I've read some papers suggesting that in some situations mutation resembling Lamarkian ideas may occur). I would agree that it is amazingly complex and difficult to understand, I just don't see a reason YET to think there is any goal behind the processes.
richjammcl 1 month ago
@richjammcl
I think that perhaps your problem with seeing teleology behind parts of life is that you're looking for overwhelming evidence. Why not look for clues instead? Certainly, the problem that the flagellum could not have plausibly arisen through purely non-teleological processes, coupled with its rational design, provide an indication that it may have been intelligently designed in some way.
Genomiques 1 month ago
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@richjammcl
I think that perhaps your problem with seeing teleology behind parts of life is that you're looking for overwhelming evidence. Why not look for clues instead? Certainly, the problem that the flagellum could not have plausibly arisen through purely non-teleological processes, coupled with its rational design, provide an indication that it may have been intelligently designed in some way.
Genomiques 1 month ago
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@richjammcl
I think that perhaps your problem with seeing teleology behind parts of life is that you're looking for overwhelming evidence. Why not look for clues instead? Certainly, the problem that the flagellum could not have plausibly arisen through purely non-teleological processes, coupled with its rational design, provide an indication that it may have been intelligently designed in some way.
Genomiques 1 month ago
@richjammcl
"The reason I pointed out the indispensability is that, if these parts are accounted for, a flagellum could function allowing for the variety of other proteins to develop over a much longer period of time..."
Yea, but since most of the indispensable proteins share no significant sequence similarity with other flagellar proteins, they almost certainly didn't arise through gene duplication...(continued)
Genomiques 1 month ago
@richjammcl
(continued from previous comment) ...so this means that even the indispensable proteins would have been co-opted. The problems with cooption as an explanation for the flagellar function are quite real, and furthermore, since these parts are still being co-opted, regardless of their indispensability, we still lack a large amount of any evidence from sequence homology for this cooption.
Genomiques 1 month ago
@Genomiques I'm not suggesting they have sequence similarity to other flagellar proteins, they have sequence similarity to other cellular proteins, that's what homology is so gene duplication is likely. If these proteins are already in the cell, it doesn't take much change for them to operate together, an advantage that would be selected for.
richjammcl 1 month ago
@richjammcl
"I'm not suggesting..."
Nor am I. But many of the flagellar proteins in Salmonella (~25%) have absolutely no sequence homologies when one BLASTs them. Thus, they have no sequence homology with other flagellar proteins, which rules out any evidence of flagellar genes being duplicated and then evolving into other flagellar genes, and they also have no sequence homology with other cellular proteins, leaving no evidence of co-option of different proteins.
Genomiques 1 month ago
@richjammcl
"If these proteins are already in the cell, it doesn't take much change for them to operate together..."
Uh, you're wrong there. Firstly, any proteins that are co-opted to form a novel molecular machine must have sufficient complementary conformation such that they are able to use energy (e.g., ATP or hydrolysis) to produce a function. There are other problems with the co-option scenario, even graver problems than the simple one above.
Genomiques 1 month ago
@Genomiques I might be misunderstanding the point you're trying to make, are you talking about needing energy to power the flagellum or utilizing energy to associate the proteins? You're undoubtedly aware that there are several domains found in countless proteins that allow them to bind and operate as a unit, diverse proteins having the necessary domains would not be surprising. The proteins performing tasks very similar to their original task but with different results is not
richjammcl 1 month ago
@richjammcl unheard of. These proteins congregating is not that far out, it happens it just typically reduces functionality rather than enhance it. I am not deluded into thinking that any random 40 proteins will form something useful but it is not a stretch to think that co-opting multiple parts to create new function is possible. Like I said, I may have misunderstood your point, but I don't see why it is a problem.
richjammcl 1 month ago
@richjammcl
"These proteins congregating is not that far out, it happens it just typically reduces functionality..."
Yes, proteins are able to bind together, but in the vast majority of cases no novel functionality results. Can you cite a single instance in the peer-reviewed literature where a novel protein machine (not cascade system!) has evolved in real-time?
Genomiques 1 month ago
@richjammcl
Consider this problem with co-option as an explanation for the origin of the flagellum:
In the above video, you will note that the ATP synthase is associated with the gated, passive pore, forming an active pore. But what if instead the ATP synthase associated with the secretin? No novel functionality would result. And this is true in the vast majority of cases so much so that the co-option is rendered an unsatisfactory explanation for the origin of molecular machines.
Genomiques 1 month ago
@Genomiques I don't see how that is a problem. Maybe such a thing did happen but no novel function resulted, this would not be chosen for. It is important to think big picture, when you have a massive number of organisms all capable of this, many would be useless or even detrimental, not surprisingly, they would not be selected for. All it takes is one to work properly and be selected for. As for citing an instance where this happened, I don't know of one. It takes a massive amount
richjammcl 1 month ago
@richjammcl of time for such a system to develop, individual proteins doing this might not be noticed after all we aren't watching every cell all of the time and it wouldn't be expected to happen regularly or on a large scale. What we have instead is instances it may have happened in the past, for example I could site the bacterial flagellum, it just hasn't been proven because it's amazingly difficult to do.
richjammcl 1 month ago
@richjammcl
"It takes a massive amount of time for such a system to develop, individual proteins doing this might not be noticed..."
Well, we've seen the real-time evolution of the PCP degradation pathway, and of nylonase, which refutes the "not watching every cell" argument. These systems are not molecular machines however; they are cascade systems. Why haven't we seen any instances of a two-part protein machine evolving? An interesting question, is it not?
Genomiques 1 month ago
@Genomiques It boggles the mind that you keep using the argument that there haven't been enough. You realize that this could have happened in a small population if everything played out perfectly right? Of course these things don't play out perfectly but that's why large populations make it more likely. The "not watching every cell argument" has not been refuted, just because we've witnessed one does not mean we've witnessed all. We have been witness to an amazingly small portion of life.
richjammcl 1 month ago
@richjammcl
"It boggles the mind that you keep using the argument that there haven't been enough."
That's because there haven't been enough. Do the calculations, instead of appealing to your incredulity (i.e., "it boggles the mind" is a sign of personal incredulity, instead of an actual biological argument).
Genomiques 1 month ago
@richjammcl
"You realize that this could have happened in a small population if everything played out perfectly right?"
Yea, and I suppose that if everything played out perfectly right then someone could win a series of poker games by every time luckily getting a royal flush. The problem is that things don't work out perfectly, and that's just not how nature works. You're appealing to your own incredulity. Let's be realistic here, instead of fanciful "perfect" hypotheticals.
Genomiques 1 month ago
@richjammcl
Consider that for a bacteria species that has only 500 different protein systems, there are 10^150 different possible two-protein system combinations (2^500). Of these different possible systems, how many will not result in any new function? If 10^50 of these combinations did result in novel, beneficial function, there are still 10^100 different non-beneficial systems that must be explored before hitting on just one beneficial one. Not enough bacteria for that.
Genomiques 1 month ago
@Genomiques I think you're misunderstanding probabilities. There is a 1/2 chance that a coin flip will land heads. There is a 1/1032 that I will get 10 heads in a row. That means that I need to flip 1032 times before it becomes likely that I will at some point in the sequence get 10 heads in a row. It is however, possible that the first 10 flips will be heads. In fact, in this case, the first 10 flips being heads is just as likely as any other sequence.
richjammcl 1 month ago
@richjammcl
"I think you're misunderstanding probabilities."
Not at all, and if I am, then so is the peer-reviewed literature.
You agree that for a pool of 500 different protein systems, there are 10^150 different possible two-protein combinations?
Genomiques 1 month ago
@Genomiques That's irrelevant. There could be 10^99999999999 combinations and that doesn't mean that two proteins that are beneficial couldn't combine in the very first cell. It takes a large number of cells before these particular combinations become LIKELY but they are still very possible. As I pointed out, I need to flip 1032 times before the outcome becomes LIKELY but it could happen in the first 10 flips. Does that much make sense?
richjammcl 1 month ago
@richjammcl
Yea, and by that logic all 42 protein components in the flagellum could have been co-opted all at once. There's a reason why Matzke et al. propose step-wise models instead of arguing that the flagellum arose by quantum co-option. Do I really need to start citing peer-reviewed papers that refute your attempt at statistics?
Genomiques 1 month ago
@Genomiques The reason stepwise is assumed is because it is more likely, it relies on a series on unlikely events rather than one massively unlikely event. It's not a difficult concept.
richjammcl 1 month ago
@richjammcl
"The reason stepwise is assumed is because it is more likely..."
Actually, the reason step-wise cooption is invoked is because the alternative, quantum co-option, is so unlikely as to be *biologically implausible and unrealistic.* That's why evolutionary biologists like H. Allen Orr repudiate quantum cooption as a general solution to the origin of molecular machines.
Genomiques 1 month ago
@Genomiques How interesting, are you suggesting that they reject one because it is implausible and accept the other in spite the fact that it is also implausible or is it more likely that they think it is plausible?
richjammcl 1 month ago
@richjammcl
They reject one because it is implausible, and accept the other because they think it is plausible. I disagree, and I have reasons for disagreeing.
Genomiques 1 month ago
@Genomiques Likelihood can refer to the unlikely. The papers I am referring to suggest that bacteria can actually induce mutation when it is beneficial to do so. I hasn't been well studied and is still somewhat on the outskirts of biology because it hasn't been proven. I don't know whether or not it actually happens, but it goes to show that we do not have a full picture when it comes to what causes mutations and how common they are.
richjammcl 1 month ago
@richjammcl
"The papers I am referring to..."
Please cite the papers. Are you suggesting that bacteria may be able to induce specific mutations at specific sites in their genomes? Is that what you're saying?
Genomiques 1 month ago
@Genomiques Unfortunately I don't have much on hand to reference but here are 2 that might be worth a look if you haven't heard of this before. Nature 335, 142 - 145 (08 September 1988); doi:10.1038/335142a0 and Science 8 June 2001: Vol. 292 no. 5523 pp. 1824-1827 DOI: 10.1126/science.292.5523.1824. As I pointed out, it is not well understood but leaves some interesting possibilities to be explored.
richjammcl 1 month ago
@richjammcl
So are you suggesting that bacteria may be able to induce specific mutations to specific genomic sites, thus possibly being an explanation for the origin of molecular machines?
Genomiques 1 month ago
@Genomiques I don't know. I'm simply saying that to assume that these things couldn't have happened because our current understanding has difficulty explaining it does not mean it didn't happen. It would be foolhardy indeed to assume we know every aspect of how these processes occur. As I said before, the only explanation for intelligence I have heard is that we don't currently understand. It's a horrible argument.
richjammcl 1 month ago
@richjammcl
"I'm simply saying that to assume that these things couldn't have happened because our current understanding....it does not mean it didn't happen."
Firstly, the suggestion that bacteria may be able to induce specific mutations to specific genomic sites as an explanation for the origin of molecular machines is a *teleological explanation,* (i.e., it's not *random* mutation any more; it's *directed* mutation, which is purely teleological). I have no problem with that.
Genomiques 1 month ago
@richjammcl
"...the only explanation for intelligence I have heard is that we don't currently understand. It's a horrible argument."
And an argument I'm not making. I am arguing that molecular machines, like flagella, by virtue of the facts that (a) there are no plausible non-telic explanations for their origin, and (b) their rational design make me very suspicious that teleology may have been behind their origin in some way.
Genomiques 1 month ago
@richjammcl
You seem to be saying that we simply don't know really how these molecular machines arose. But if that is what you are saying, then the co-option explanation is not the default explanation, and a teleological explanation should be opposed no more than a non-teleological explanation, unless one is more robust. The rational design inherent to the core flagellar structure is positive evidence in favor of the telic view.
Genomiques 1 month ago
@Genomiques (a) Again, there may not be any plausible non-telic explanations that we know of but that doesn't mean there aren't any, that's not an argument. (b) Appearance of design does not necessarily suggest design. Looking at the beautiful lattice of salt crystals might suggest they were crafted by little artists but there is no reason to think that they are not governed by the same principles that create any other crystals.
richjammcl 1 month ago
@richjammcl As I've pointed out, I wouldn't rule out design, it is possible. In terms of which hypothesis is more robust; One relies on natural forces and processes at least some of which are known and many are well understood. The other relies on a prime mover and again, saying this thing looks like something that one might design is not the same as saying this could not have not been designed. We have no evidence for this designer apart from the appearance of design which we don't
richjammcl 1 month ago
@richjammcl even know is or is not designed yet. Given that we can't realistically tell the difference, I fail to see how appearance of design could ever be considered evidence.
richjammcl 1 month ago
@richjammcl
I'm not even arguing from appearance of design. Whatever gave you that idea? The telic hypothesis is just as robust as the non-telic hypothesis. You might want to look into the front-loading hypothesis, an inherently telic hypothesis, and it is very testable.
Genomiques 1 month ago
@Genomiques An interesting theory, are you suggesting panspermia then? It certainly seemed like you were toting the importance of appearance of design. It might be helpful to point out how you could possibly discern between something that was "rationally designed" and something that was not rationally designed but has purpose.
richjammcl 1 month ago
@richjammcl
"An interesting theory..."
Not meaning to be pedantic, but you mean *hypothesis.* Front-loading is a bit like panspermia, I suppose, but I think panspermia doesn't necessarily entail teleology. Panspermia, as I understand it, simply posits that the first life forms on earth came from outer space. The front-loading hypothesis goes one more step ahead from this, and suggests that earth was seeded with life that had the genes to shape subsequent evolution.
Genomiques 1 month ago
@richjammcl
"In terms of which hypothesis is more robust...one relies on natural forces..."
Uh, teleology also relies on natural laws. You yourself acknowledged, implicitly at least, that bacteria may be able to induce specific mutations at specific genomic sites, thereby being able to explain the origin of molecular machines. This is a purely teleological explanation, and your problem with this telic explanation is?
Genomiques 1 month ago
@Genomiques Perhaps we mean different things when we talk about design. I'm not sure if you looked at the papers I referenced but they don't suggest that bacteria decide that x is beneficial so I'm going to mutate to do that. There may be processes at play which, when confronted with death, bacteria induce mutations at a greater rate increasing the likelihood that one in a colony will have the required mutation and will then repopulate the colony, the rest of whom will be dead.
richjammcl 1 month ago
@richjammcl
"There may be processes at play which, when confronted with death, bacteria induce mutations at a greater rate..."
Oh, well, if that's one of your solutions to the origin of molecular machines then it's not at all that great. Simply accelerating the mutation rate doesn't offer a solution to the origin of molecular machines if these mutations are specified.
Genomiques 1 month ago
@Genomiques One of your issues is that there hasn't been enough bacteria for this to occur, massively increasing mutation rate means that there are considerably less bacteria needed before this becomes likely. And again, something does not have to be extremely likely to happen, only plausible.
richjammcl 1 month ago
@richjammcl
"One of your issues is that there hasn't been enough bacteria for this to occur, massively increasing mutation rate means that there considerably less bacteria needed..."
Yea but there is a maximum possible mutation rate before mutation rates become lethal. The mutation rates of viruses are near the maximum mutation rate, so you can't get any "faster" than the mutation rate that becomes lethal. I'll try to get the PNAS paper on that: can't think of what the title was.
Genomiques 1 month ago
@Genomiques Of course if you let mutation run free you will inevitably destroy your genome and die. However, on a large scale, increasing mutation rate means a large number of mutations without any one organism reaching particularly high mutation rates. Many, if not most of the organisms involved would not receive anything useful and might even die but on occasion, you will receive the mutation you need. Putting a colony of bacteria on a medium rich in antibiotic shows how,
richjammcl 1 month ago
@richjammcl while most organisms will die, some will have a beneficial mutation and survive. They quickly reproduce and, to an untrained eye, it appears that the bacteria were unaffected by the antibiotic. Of course that's not the case, just a massive amount of dead bacteria were replaced with new, more fit bacteria. All it takes is one bacteria to receive a beneficial mutation and it can outperform its brethren.
richjammcl 1 month ago
@richjammcl
For example, if an ATP synthase can, via a mutation, associate with a passive pore, there is nothing stopping it from associating with another ATP synthase, a secretin, an ion channel, an adhesive protein, etc. In other words, the ratio of mutations that will result in a novel molecular machine versus those that will not result in beneficial function is far different than the case with antibiotics.
Genomiques 1 month ago
@Genomiques That's fair, but if it has the ability to associate with all of these things and one is useful, this organism will be selected for. Granted, much of its progeny will have a minimal advantage, but an advantage none the less. From that point, specificity can be developed. Keeping in mind that, while the whole motor wouldn't appear over night in one organism, it is possible that multiple steps were in development at the same time, yet another way that the minimal amount of
richjammcl 1 month ago
@richjammcl bacteria and time is less. On top of these things, organisms have systems in place to minimize mutation rates because it is so often detrimental but if we're looking at bacteria before basic motility was achieved, we're going back in time to a point where its ability to correct mutation would have been less efficient. Mutation would have been more common and accelerating these pathways is hypothetically possible.
richjammcl 1 month ago
@richjammcl
"...but if we're looking at bacteria before basic motility was achieved, we're going back in time to a point where its ability to correct mutation would have been less efficient."
This is circular reasoning in its most blatant form. Because you have non-teleological filters on, you're assuming that the proof-reading machinery of the cell had to evolve its efficiency. Thus, you're making an assumption that proof-reading machinery was less efficient in the past.
Genomiques 1 month ago
@Genomiques And you're assuming that it didn't. If this wasn't an assumption you're making you wouldn't be able to say there haven't been enough bacteria in existence because we would know little about how often mutations occurred in early life.
richjammcl 1 month ago
@richjammcl
Even if mutations occurred at an unprecedented rapid rate, it still doesn't solve the problem.
Genomiques 1 month ago
@richjammcl
You rely way too much on bacteria population sizes and mutation rates. But if a cell has only 500 different protein systems, how many 2 protein combinations are possible? A total of 10^150. Of these, the vast majority will be non-beneficial combinations. Even being extremely generous and assuming 10^50 will be beneficial, that still leaves 10^100 combinations to be explored before it's likely a single beneficial system will arise.
Genomiques 1 month ago
@Genomiques Of course I rely on population sizes, they're a necessity. For example, it is incredibly unlikely that if I buy a lottery ticket that I'll have the winning numbers. That doesn't mean that no one wins the lottery, it happens regularly. Granted we're talking about statistics many orders of magnitude larger but we're also dealing with populations many orders of magnitude larger.
richjammcl 1 month ago
@richjammcl
You forget that there are far, far more possible two-protein combinations that will not be beneficial than there are combinations that will be beneficial. If any ATP synthase can associate with those proteins, nothing is stopping those proteins from ALSO associating with each other, with no beneficial result.
Genomiques 1 month ago
@Genomiques Given that many of these proteins existed pre-flagellum, it is possible that the mutation was for specificity and not random binding properties that allowed the protein to interact with anything in it's path.
richjammcl 1 month ago
@richjammcl
"Given that many of these proteins existed pre-flagellum, it is possible that the mutation was for specificity and not random binding properties..."
That's not the point. If it can have a specific mutation that allows it to bind with one protein, there's nothing stopping it from having mutations that would allow it to bind with other proteins, even though these interactions wouldn't result in novel function.
Genomiques 1 month ago
@Genomiques Of course there's nothing stopping that! As I have said multiple times, there were undoubtedly countless mutations that were useless and countless more that were deadly, the point is that when one that is beneficial occurs, it is selected for and that organisms progeny multiply and go on to have many more useless mutations until one of them has a beneficial mutation and it happens again. There are many losing lottery tickets, you don't hear about the many many people who
richjammcl 1 month ago
@richjammcl didn't win the lottery you hear about the one that does. It only takes one.
richjammcl 1 month ago
@richjammcl
"...the point is that when one that is beneficial occurs.."
Right, and what if the ratio of beneficial/non-beneficial protein combinations was 1:10^100. This means that 10^100 combinations will be explored before any one beneficial combination will occur. Not so with the lottery. With the lottery, the ratio of win/no wins might be 1: 1,000,000. So if one million people buy lottery tickets, one will win.
Genomiques 1 month ago
@Genomiques Even if you're ratio of 1:10^100 is correct, and I don't think that it is, you don't have to go through all 10^100 to find the right one. If there are 10 balls in a bag and only one is red and that's the one I need, there is no reason for me to keep looking if the red one is the second ball I pull. This is broken math, 1:10^100 does not mean it will take 10^100 mutations to get the right one.
richjammcl 1 month ago
@richjammcl
"1:10^100 does not mean it will take 10^100 mutations to get the right one."
Yes, it does, unless some cell is extraordinarily lucky - and that's appealing to miracle, not to biotic reality. That's why the odds of a given function evolving decreases exponentially the more gene products are required for that function (and assuming no intermediates are functional).
Genomiques 1 month ago
@Genomiques For example, the odds of winning the 6/49 are 1:13,983,816. That means if you play every week, it takes 13,983,816 weeks before you are LIKELY to win the lottery. Some how, people win the lottery on a regular basis however. By the same logic though, they haven't played enough times for this to happen. It's just wrong.
richjammcl 1 month ago
@richjammcl
"That means..."
The ratios are different here. Millions of people buy lottery tickets, making the *total ratio* wins/no wins different. The odds of ONE person winning the lottery is 1:13,983,816, but that *someone* in a pool of a million people wining is 1,000,000:13,983,816.
Genomiques 1 month ago
@Genomiques Exactly, hence the large populations of bacteria referred to previously. "Yes, it does, unless some cell is extraordinarily lucky" if you honestly think that you don't understand basic probabilities. There's a 1/6 chance that I'll roll a 4. That doesn't mean that I need to roll 6 times to get a four and it doesn't mean anything remotely strange happened if my first roll was a 4. I'm not saying that the mutation required happened the first time every time, that would
richjammcl 1 month ago
@richjammcl ridiculous but to think it happened the 10^100th time every time is equally ridiculous. It might have happened the first time, the 50 000th time the 10^62 time or the 10^100 time, all of which are equally likely unless there is some process at work to keep it from happening.
richjammcl 1 month ago
@richjammcl
"...all of which are equally likely unless there is some process at work to keep it from happening..."
Too bad the peer-reviewed literature - and basic logic - disagrees with you.
Genomiques 1 month ago
@richjammcl
I can bring up many instances where probabilities are applied in the way I am applying it, from the peer-reviewed literature. Furthermore, if your logic was correct, then a basic argument for common descent - nested hierarchical patterns that result from protein sequence alignments - falls apart, simply because one could, by your logic, argue that this pattern is merely the result of chance. After all, all patterns are equally likely. You're misunderstanding probability.
Genomiques 1 month ago
@Genomiques Peer review has been wrong before, people often make simple mathematical mistakes. Let's make this very simple, when rolling a dice, is any one number more likely than the others? No. There is a 1/6 chance for each. If I roll a 1, is that strange? No. Any of the other numbers? No. So even though there is a 1/6 chance in rolling any one number, one of the numbers has to be rolled. Therefore one of the numbers came up earlier than you were expecting if you
richjammcl 1 month ago
@richjammcl were expecting it to take six rolls. With protein compatibility, even if it was a 10^100 chance, if one of those mutations happened it obviously did not take 10^100 mutations. If all mutations are equally likely, the beneficial mutation could come up anywhere in that sequence could it not? I fail to see why that is confusing for you.
richjammcl 1 month ago
@richjammcl
When I align DUTpase of E. coli and Salmonella, there is ~92% sequence identity. From this I can reasonable conclude that the two sequences share a common ancestor. However, by your logic we could just as reasonably conclude that that sequence identity was the result of chance, true? I wonder why every biologist would disagree with you.
Genomiques 1 month ago
@Genomiques It is hypothetically possible but, as the number of steps increase, the odds decrease. For example, if I rolled a 6 it wouldn't be surprising if my next roll was also a 6. By contrast, if I rolled 43242342134234234235153142342353256 in succession the rolled 43242342134234234235153142342353256 again it would be surprising. It is just as likely as any other individual sequence but there are more different sequences than identical, that's what makes it unlikely.
richjammcl 1 month ago
@richjammcl
"It is just as likely as any other individual sequence, but there are more different sequences than identical, that's what makes it unlikely."
Exactly. There are far more non-beneficial combinations than beneficial protein combinations, that's what makes the co-option scenario an unlikely explanation for the origin of molecular machines like flagella.
Genomiques 1 month ago
@Genomiques It feels like we're just spinning in circles now. If you're interested in the probabilities I was trying to explain earlier that you think don't make sense, I'd recommend a book called Innumeracy, it's about common mathematical mistakes we often make. Ultimately I think we're just disagreeing about what we personally consider plausibility. Regardless, there are countless unlikely events that occur every day without anyone forcing them to happen.
richjammcl 1 month ago
@richjammcl
"Regardless, there are countless unlikely events that occur every day..."
Then, by definition, they're not unlikely o.O
Genomiques 1 month ago
@Genomiques What!? You think that once something happens it becomes likely? Flipping a coin 1000 times and getting 1000 heads is unlikely. If I did it, it's something unlikely, happening. It is still unlikely.
richjammcl 1 month ago
@richjammcl
Anyways, you really don't seem to be grasping my point. Flagellar evolution is unlikely for the same basic reason that it's unlikely for two unrelated sequences to converge, by chance, into nearly identical sequences.
Genomiques 1 month ago
@Genomiques I really don't see how those two scenarios are remotely similar.
richjammcl 1 month ago
@richjammcl
"I really don't see how those two scenarios are remotely similar."
Then WHY is it unlikely for two unrelated sequences to, by chance, happen to have nearly the same sequence identity? The answer to that question is my answer to your arguments over probability and co-option.
Genomiques 1 month ago
@Genomiques One requires two long identical processes. That is unlikely. One process is comparatively far more likely. Even if we are dealing with very improbable events, it is unlikely to happen but exponentially less likely to happen twice in the same way. There is convergent evolution but that produces two different structures with similar function not two identical structures.
richjammcl 1 month ago
@richjammcl
"One requires two long identical processes."
Yes, BUT by your argument, one sequence matching another sequence is just as likely as any other sequence. I'm not talking about convergent evolution here because that would no longer be pure chance: natural selection would be in the equation.
Genomiques 1 month ago
@Genomiques yes, both are equally likely but in the case of two systems, there are more possibilities. For example, rolling a 6, 1/6. Rolling 2 dice and them both be 6, 1/36. The six is just as likely on each die and they don't influence each other but there are more possibilities so it becomes less likely.
richjammcl 1 month ago
@richjammcl
"...but there are more possibilities so it becomes less likely."
Yes, AND there are far more possible protein combinations that are not beneficial than there are protein combinations that are beneficial, so the latter is less likely.
Genomiques 1 month ago
@Genomiques Are we seriously going over this again? I have already conceded that a useless of damaging mutation is more likely than a beneficial one. Natural selection is a mechanism by which that doesn't matter. You can have negative mutations all you want, you'll die and that's the end of it. If you have a beneficial mutation you procreate. There have been countless detrimental mutations over the years, those organisms die. That's the idea.
richjammcl 1 month ago
@richjammcl
"I have already conceded that a useless or damaging mutation is more likely than a beneficial one."
Yes, and at the level of molecular machines, by even the most generous estimates, non-beneficial mutations are 10^100 more likely than a single mutation that would associate two proteins that would just happen to form a novel function.
Genomiques 1 month ago
@Genomiques Where are you getting your numbers from?
richjammcl 1 month ago
@richjammcl
Refer back to my estimates. With 500 different protein systems, there are 2^500 = 10^150 different possible two-protein combinations. Of these, the vast majority will be non-beneficial. Even assuming that 10^50 of these protein systems will be beneficial, this still means that for every beneficial protein system, there will be 10^100 non-beneficial systems.
Genomiques 1 month ago
@Genomiques That is assuming that many other potentially useful combinations are not useful because they haven't occurred. Regardless, it completely ignores things such as, proteins that function in proximity are far more likely to interact than proteins that are not, it assumes that all proteins are equally likely to associate which might not be the case. Its not like we're throwing a pile of Lego together and seeing what sticks, not all proteins are created equal.
richjammcl 1 month ago
@richjammcl
"That is assuming...because they haven't occurred."
Not at all. Regarding your other points:
a) Proteins that function in proximity are not far more likely to interact *through virtue of mutation.* They may interact with proteins in close proximity, through chemical bonds, etc., but if this association is not genetical than it's not evolutionarily meaningful.
b) Name one reason why proteins would not be equally likely to association with each other.
Genomiques 1 month ago
@Genomiques That is an assumption you're making, there could be countless that just haven't occurred that you're passing off as detrimental. a) If a protein has a mutation that gives it the ability to bond to another protein, it is absolutely more likely to interact with a protein it comes into contact with rather than one it does not come into contact with. b) For exampleif a protein has one spot to dock vs multiple, their docking sites could be more or less available to the outside
richjammcl 1 month ago
@richjammcl
Yea but:
a) A protein is just as likely to have a mutation that allows protein-protein binding as it is to have a mutation that localizes it to another subcellular location, thus making it capable of binding with proteins it previously did not interact with.
b) I don't see how this makes protein X more likely to associate with protein Y than with, say protein Z. Elaborate.
Genomiques 1 month ago
@Genomiques a) again, if the protein mutates and does something that is not needed it is not chosen for. b) If protein x has a new binding domain that allows it to interact with either Y or Z but Y has multiple binding sites and Z has one, it has a better chance of binding to Y. It might still bind to Z but with less frequency. Increased specificity will be selected for. Lets say for the sake of argument that binding to Y is beneficial and Z is detrimental. If the benefits are
richjammcl 1 month ago
@richjammcl roughly equal to the detriment but binding to Y happens considerably more often than to Z, this is something that can be selected for. After this point, increased selectivity can be selected for because, naturally, having the benefit alone is better than the benefit and detriment together.
richjammcl 1 month ago
@richjammcl If it can bind to a binding site on both Y and Z but Y has a binding site on the outside and Z has a binding site somewhat blocked by protein structure, it is more likely to bind to Y.
richjammcl 1 month ago
@richjammcl
a) This part of your argument is irrelevant to what we're currently discussing: whether a protein is just as likely to bind to one protein as to another.
b) This argument of yours is reasonable, but it doesn't really affect my core argument significantly since in most cases, a random protein will be just as likely to bind to a protein than to another, except in the few cases where a given protein has more binding sites.
Genomiques 1 month ago
@Genomiques a) This is relevant. Although there are a huge number of proteins in any given cell, there are a limited amount that each protein will come into contact with. A protein could mutate in such a way that if it were to bind to any number of proteins it would be catastrophic. If the protein never comes into contact with these proteins and does come into contact with a beneficial one, that damaging mutation is anything but. b) Although that is true, it does
richjammcl 1 month ago
@richjammcl limit the number of proteins that a mutated protein might bind to. Since the argument we are discussing is that there are a massive amount of proteins that a protein could interact with, limiting the number is relevant.
richjammcl 1 month ago
@richjammcl
You know what, I think that this discussion can hardly be resolved in the 500 character limit of YouTube, and so I'll put together a video on cooption in the next week or so, where I'll use animations et al. to try to get my point across. If you wish to continue this discussion that's fine, but I think at the moment you might be more interested in discussing this: what biological feature would make *you* suspicious that teleology played a role in the history of life?
Genomiques 1 month ago
@Genomiques Difficult to say really. I don't think it would be any one feature. As I see the argument it is that we don't understand how it happened so maybe there's a designer. Or, I suppose, your variety is somewhat closer to it seems so improbable that I suspect a designer. I think that's the wrong way to go about it personally, seems backwards. I would be interested in seeing how this front loading idea plays out. I'm not sure how it would prove design, but I think it
richjammcl 1 month ago
@richjammcl at least has the massive advantage over most ID claims in that it's testable. That's how real science works, take a claim and try to prove it wrong, see what's left standing at the end of the day instead of throwing our hands up and saying it couldn't have happened that fast in that population because that doesn't make sense to me.
richjammcl 1 month ago
@richjammcl
At the moment, I'm not looking for proof of teleology. I'm looking for the clues and the evidences in favor of the front-loading hypothesis. There are several ways to test the front-loading hypothesis, and if it's predictions are confirmed, then it is considerably strengthened. Of course, nowhere in this discussion do we mention any gods. Anyone who assumes the intelligence must be supernatural by any means is clearly not that acquainted with the workings of science.
Genomiques 1 month ago
@Genomiques Yeah, the problem it would have is much the same as abiogenic hypotheses, even if you can make it happen it is still only a possibility. Abiogenesis is an interest of mine and it can be quite frustrating playing in that arena. In regards to your question, I'm not sure there is a feature that would make me suspicious. It's always a possibility in the back of my head because I can't think of a way to disprove it, but never the less, it wouldn't be my go to explanation for
richjammcl 1 month ago
@richjammcl anything. I find the idea of directed panspermia quite interesting and I think we'll very likely pull it off ourselves but I haven't seen anything that would make me think it's any more likely than the other ideas at hand. A bit of Occams razor I suppose, we just see the cut a little differently.
richjammcl 1 month ago
@richjammcl
Would like to continue this discussion, but right now I've gotta catch a wink of sleep. A belated Happy New Years to you :P
Genomiques 1 month ago
@Genomiques Haha, and to you. I just looked and we've taken up the past 16 pages of comments. Perhaps this conversation would be more appropriate for inbox messages.
richjammcl 1 month ago
@richjammcl
I agree. I'll send you a message to your inbox as soon as possible, on front-loading and how we can test it - if you're interested in that. I'll try to do that tomorrow, 'cause right now I'm kinda busy. Have a good evening.
Genomiques 1 month ago
@richjammcl
Remember, I'm not necessarily talking about evidence in the sense that it would convince you of that teleology played a role. I'm talking about clues. What kind of clues would make you a bit suspicious? By the way, I do not conclude teleology solely on the basis of a lack of a non-telic explanation. Rather, the lack of a non-telic explanation is just one factor that shifts the balance in favor of the telic hypothesis.
Genomiques 1 month ago
@richjammcl
"...it is possible that multiple steps were in development at the same time..."
It's not all that likely that multiple steps were in development in the same bacteria population.
Genomiques 1 month ago
@richjammcl
Yea but accelerating the mutation rate still doesn't solve the problem. Even if you increased the mutation rate to every thousandth nucleotide being mutated, the problems with evolving a molecular machine are still very real. Resistance to antibiotics evolve quickly enough because only a few point mutations are needed. With chloroquine resistance in malaria, just one point mutation will be beneficial. Things are different with molecular machines.
Genomiques 1 month ago
@richjammcl
Found it. See: "Protein stability imposes limits on organism complexity and speed of molecular evolution." Doi: 10.1073/pnas.0705366104.
Genomiques 1 month ago
@richjammcl
"Appearance of design does not necessarily suggest design."
It does *suggest* design, but it is not in itself positive evidence of intelligent design. Rational design, however, is a hallmark of rational minds and thus it is positive evidence in favor of the telic hypothesis. The discontinuity of the flagellum from things known to be able to have evolved, *coupled with its rational design* is at least a clue that teleology might be at play here.
Genomiques 1 month ago
@richjammcl
Anything with a probability above 0 is POSSIBLE. It is *possible* that I will win a poker game by getting a string of royal flushes in a row. But *possibility* should not be confused with *plausibility.* Of course, the odds of the flagellum evolve through cooption are above 0, thus it is possible. But it's not biologically *realistic.*