All your are showing is that evolution is unfalsifiable, everytime something hapens to be inconsisten with the tree pttern predicted by evolution, you will use this kind of excuses.
mammals do not share ervs with other classes of animals this is why we will never find an ERV in ducks chimps but not in humans.
@Answerquestions1 No, LIAR, this doesn't "happen to be inconsistent," it ISN'T INCONSISTENT!
"mammals do not share ervs with other classes of animals"
Yes they absolutely do!
"this is why we will never find an ERV in ducks chimps but not in humans."
WRONG: Evolution HAPPENED, and that's why we will never find an ERV in ducks chimps but not in humans--because it violates the nested hierarchy--but we WILL find ERVc in chimps and humans AND ducks!
please show me an orthologs erv that mammals share with other classes.
btw, ervs that humans lack have been found in chimps and monkeys. so you can no longer use ´´recnt incertion´´ as an excuse (as you did in your video)
@Answerquestions1 For HUNDREDS of examples, across aves, mammals, crocodiles, and many other large-scale groups, see "Distribution of Endogenous Retroviruses in Crocodilians," Journal of Virology, 83(19): 10305-10308 (in particular, Fig. 1 on page 10306)
@Answerquestions1 Here's another source: "Viruses and the evolution of life" by Luis P. Villarreal
From p.335: "Overall, we see evidence of lineage-specific ERV colonization in all vertebrates, well before the evolution of placental species. These early ERV colonizers are still maintained, typically in small numbers. Additionally, much more numerous and specific ERV colonization events have occurred...species lineages can be distinguished on these later ERV colonizations."
ATTENTION:(TheRationalizer) - Your feeble and immature act to block me and use of the 'F' word shows clearly YOUR inability to discourse with those who don't agree with you. Your 'threat by proxy' excuse is just 'that' - you are a coward and others on youtube should know your unfairness is ongoing! --WEAK -- ! ! ! ! ! !
0:40-0:52... caught that... i may not have the book info you have on this... but know when you insult... like so many you start with the insults first
@IloveYOUviruses The nested hierarchy and how alleles work was NOT made up after the fact to suit this! This exact scenario IS a prediction of the model!
It's the ignorance of you pathetic creationists that is laughable.
@shanedk Still, this is not an explanation of differences in "ERVs" but an excuse, the only evidence that some ERVs dissapeared is that otherwise it would destroy evo "theory" (again), that only counts for the relligious deluded evo heads
@shanedk Who said that ERV "appears"?? are you using the conclusion to prove the conclusion? Oh yeah, I forgot that you are the one who lied about whales evolution and Berlinsky. woah! lies and excuses plague this channel!
@IloveYOUviruses Look, IDIOT, we KNOW that ERVs appear because WE'VE SEEN IT HAPPEN! EVERY organism that gets a retrovirus (such as HIV-1, HTLV, or FLV) has the retrovirus's genome incorporated into the nucleus of the cell it attacks. That's what a retrovirus IS!!!
HOW DARE YOU accuse others of lies and excuses when YOU YOURSELF haven't even done the BASIC amount of research needed to talk about it! You creationists are the most dishonest, immoral people I ever meet!
“Who said that ERV "appears"?? [Are] you using the conclusion to prove the conclusion?”
The hallmark of an insertion is a displacement of chromosomal DNA, and the hallmark of insertion by integrase is the presents of target site duplication, due to the way it attacks the 5' and 3' phosphodiester bonds with an offset of a few base pairs.
Since ERVs are accompanied by target site duplications and DNA displacement, they are necessarily endogenized/fixed insertions. Combine that with their configuration of U3rU5-(pbs)-gag-pol-env-(ppt)-U3rU5, and it is undeniable that the insertions are proviral.
@MolecularBioVids2 LOOK, IF YOU WANNA IMPLY THAT ERVs ARE JUST... lol Im just kiddin, I really admire how you avoid hate-speech and name calling like that shanek guy
thanks for using real science, let me I ask to you: who says that ERVs insert at random locations?
Cuz according to Taruscio et al:
"The present results indicate that there are highly specific integration patterns for each endogenous retrovirus that do not readily relate to their sequence or particle classification..." (1991)
“[Who] says that ERVs insert at random locations?”
Firstly, we know that insertion is nonspecific on the nucleotide level, due to the way it directly attacks the bonds, with no need to ligate. Yes, different retroviral integrases have biases (+/-) for an array of general genomic areas, but insertion still takes place elsewhere—just not as frequently. So, relative to pure randomness, insertion is highly specific, but relative to locus specificity, insertion is highly random.
This is also pointed out in the Taruscio (1991) paper:
"Retroviruses have the ability to integrate into the genome of their host, in many cases with little apparent sequence or site specificity. However, relatively few studies have addressed more general features of chromosomal integration... These investigators have suggested that higher order structural features, or an active transcriptional capacity of chromatin may be fundamental for preferred integration events (p.141-142)."
The number of species that share ERVs in orthologous loci requires downright locus specificity on the nucleotide level for the observed sharing to occur via separate insertion in distinct lineages. Given this requirement, and given the large number of species (all primates, for instance) that share ERVs in orthologous loci (Anderssen et al., 1997), the model of uncommon ancestry is falsified and inheritance from a common ancestral species is necessitated.
Secondly, even if insertion were locus specific, the only way that the hierarchical sets could arise is if infection susceptibility varied precisely with genetic commonality and if all species were infected, regardless of geographic isolation. Not only does the observed distribution of ERVs show this not the case (Polavarapu, Bowen, & McDonald, 2006; Yohn et al., 2005), but the restriction capability of the innate immune system also shows no such pattern (Kaiser, Malik, and Emerman, 2006).
@MolecularBioVids2 Taruscio et. al noticed that there was little research on that topic (integration preference) so they estudied 3 kinds of ERVs and realizad that "Each retroviral sequence exhibited a unique and markedly different integration pattern.", *IF* there is preference for integration, the NH argument is pointless, maybe nothing more than a good circular guess.
Please, tell me if Taruscio was wrong back at the 90's, did he lied? Is he just an amateur? What happened?
@IloveYOUviruses if we can't get over a paper from 1991 it would be pointless to touch the more recent topic of the thousands of (somehow) very useful ERVs.
@MolecularBioVids2 "Because there are 50-1000 copies of each of these retroviruses in the genome, it was possible to evaluate repeated integration events. Each retroviral sequence exhibited a unique and markedly different integration pattern... The present results indicate that there are highly specific integration patterns for each endogenous retrovirus that do not readily relate to their sequence or particle classification."
I have not twisted it at all. Please read and what I said again. Once again, the preference reported in the Taruscio study is for the general proximity of “higher order structural features;” not between specific base pairs (loci). Insertion was known to be nonspecific on the nucleotide level then, and subsequent study has confirmed this, as well as confirmed the high order preference. This does not explain ERVs shared at specific loci.
@MolecularBioVids2 Mitchell didn't refuted Taruscio, he worked with other ERVs and proved that some ERVs can be more biased than others, besides, Mitchel's team used strains derived from pathogenic viruses wich are known to be dangerous (obviously!) unlike the thousands of (somehow) very useful ERVs... which reminds me...
“Mitchell didn't [refute] Taruscio, he worked with other ERVs and proved that some ERVs can be more biased than others...”
Firstly, I explicitly stated that The Mitchell study corroborated the Taruscio study. Secondly, the Mitchell study showed not only different levels of bias, but also entirely different biases; and I never contradicted what you just said.
“...besides, [Mitchell's] team used strains derived from pathogenic viruses [which] are known to be dangerous (obviously!) unlike the thousands of (somehow) very useful ERVs...”
As I already explained, components of proviruses are sometimes co-opted, and the remainder left to mutate to the point that they lack virulence. And the Mitchell study was mealy an assessment of the operation of viral integrase. Arguing about virulence is a non sequitur.
@MolecularBioVids2 ...that you seem to be confused, I never said ERVs were totally useful, we don't know that, neither we know that "There are no truly functional ERVs" or "there are only functional components.", that would be the same error as those who said that 95% of the DNA was junk and then one guy discovered it wasn't, patented it and got disgustingly rich, this kind of reasoning has always been detrimental to science, be careful.
“...I never said ERVs were totally [useful;] we don't know [that;] neither [do] we know that ‘There are no truly functional ERVs’ or ‘there are only functional components...’”
By ‘none’ and “only,” I am strictly referencing the data collected thus far. All current observations indicate what I said. These data indicate exaptation and scaffolding. Thus my point still stands that “functionality is simply a red herring, when discussing how ERVs necessitate common ancestry.”
@IloveYOUviruses Even if this phantom "pattern" of yours actually existed, that would still mean that a retrovirus would have AT BEST a 1 in 600,000,000 chance of inserting itself at a particular location in the human genome. Doesn't help you.
“[A. B. Conley et al.] show that ERVs are involved in the transcription on 1/5th of the genome, that's way too much for a random insertion and clearly shows a pattern.”
As stated in the Conley study, “approximately 5% of the human genome sequence is derived from retroviruses (p.1563).” The reference they give is the ‘Initial sequencing and analysis of the human genome’ paper, which states that 2.03×10^5 class I/II/III ERVs comprise 4.64% the human genome (Lander et al., 2001).
The “51,197 ERV-derived promoter sequences that initiate transcription within the human genome (Conley, 2008, p.1563)” represent only 25.2% of total insertions. Add to that leaky transcription, and the fact that truly beneficial insertions can subsequently be subjected to directional selection, and the observation that “PET tags that capture transcripts initiated from ERVs cover 22.4% of the genome (p.1566)” doesn’t contradict observations of nonspecific nucleotide level insertion.
“And about targeting sequences, that's a well documented topic, and I admit, the bias depends [on] the ERV. [With] all that info, ERVs+NH is just a good circular hope.”
I’ve already explained how none of this indicates locus specificity. But you need to understand that even if it did, it doesn’t even begin to explain the hierarchical grouping of shared ERVs. For the third time:
Even if insertion were locus specific, the only way the shared ERVs could be hierarchically grouped, and also the result of parallel integration, is if infection susceptibility to vary precisely with genetic commonality, and for precise species-wide infection, regardless of geographic isolation.
The observed distribution of ERVs and the observed variation in restriction capability of the innate immune system each result in no such grouping; thus they falsify the parallel integration hypothesis.
Another thing that the parallel integration hypothesis utterly fails to explain is the positive correlation between number of species that share orthologous ERVs and the discontinuity between the 5’ and 3’ LTRs of those ERVs. It also doesn’t explain the sharing of mutations between orthologous ERVs’ LTRs, the hierarchical grouping of such mutations, or that the nested hierarchies of distribution match those of mutation.
Examples include viral LTRs replacing or augmenting a gene’s preexisting promoters (Cohen, Lock, & Mager, 2009), or enJSRV env and gag genes contributing to placental growth/differentiation regulation (Dunlap et al., 2006; Palmarini et al., 2000) and causing gag-gag interaction that restrict pathogenic JSRVs (Mura et al., 2004), respectively. There are also very few ERVs that are even in a configuration and/or position that they can contribute any function.
That it is only a few functional components from a small percentage of ERVs is not only positive evidence that the functions were co-opted, rather than designed in, but it falsifies the idea that ERVs exist solely to benefit the host organisms, that ERVs were designed in genomes from the beginning, and that shared ERVs must be designed there to confer a similar benefit.
But it gets worse; even this evidence is a moot point, because we know that ERVs are proviral insertions that have been endogenized and fixed in populations. We know this due to their sequences and due to the presence of DNA displacement and target site duplication. [refer to the first two posts I made to you for a detailed explanation]
This more than falsifies the idea that ERVs were designed in, since the fact that they are insertion means that there was a time when the organism existed in some form without them, prior to their insertion.
Any functional components are necessarily post-insertion exaptations, and the fact that they are necessarily insertion means that they can not be part of any 'original design.' The issue of functionality is simply a red herring, when discussing how ERVs necessitate common ancestry.
@IloveYOUviruses Oh, come on--in 1991 they didn't even know enough to make the antiretroviral drugs we have today that have stopped making AIDS the death sentence it once was! They barely had transcriptase inhibitors. A LOT has been learned since then. 20 years is a LONG time in science.
“Taruscio et. al noticed that there was little research on that topic (integration preference) so they [studied] 3 kinds of ERVs and [realized] that ‘Each retroviral sequence exhibited a unique and markedly different integration pattern.’... Please, tell me if Taruscio was wrong back at the 90's, did he [lie?] Is he just an amateur?”
Dr. Taruscio was correct, and continued research over the past couple decades confirms her findings. But you are misunderstanding these findings:
The ‘preferences’ are merely minor statistical biases for or against insertion within the very general areas of “chromosomal regions rich in expressed genes… [their interwoven] CpG islands… active genes… [and areas] near transcription start sites (Mitchell et al., 2004),” but these biases are so minor, that they require thousands of trials (3127 used in the Mitchell study) just to detect them. And insertion still occurs out of the preferred areas—just with decreased frequency.
And that is merely the “higher order structural” level—it remains true that insertion is nonspecific on the nucleotide level. When Dr. Taruscio says “unique and markedly different integration [patterns],” she is referencing the distinct differences in the deviation from randomness. And again the findings are consistent with the fact that, relative to pure randomness, insertion is highly specific, but relative to locus specificity (nucleotide level), insertion is highly random.
“*IF* there is preference for integration, the NH argument is pointless, maybe nothing more than a good circular guess.”
That is quite inaccurate. Again, the number of species that share ERVs requires locus specificity, for the observed sharing to occur via parallel integration. The preferences are nowhere near that. Thus the large number of species that share ERVs falsify the parallel integration hypothesis, and necessitate common ancestral species.
And (also) again, even if insertion were locus specific, parallel integration requires infection susceptibility to vary precisely with genetic commonality, and for precise species-wide infection, regardless of geographic isolation.
The observed distribution of ERVs and the observed variation in restriction capability of the innate immune system each falsify the parallel integration hypothesis.
“Still, this is not an explanation of differences in ‘ERVs’ but an excuse, the only evidence that some ERVs [disappeared] is that otherwise it would destroy evo ‘theory’ (again), that only counts for the [religious] deluded evo heads.”
Although patterns are formed and act as powerful evidence of past occurrences and of mechanisms that causes them, the complex nature of the physical world (due to so many simultaneous interactions on so many levels) often causes deviation from those patterns.
Thus the patterns act as indicators of what is actually going on, and deviation from them is both expected and rendered likely not indicative of what is actually going on.
Since HERV-K-GC1 is the only known deviation from the distributional nested hierarchy of ERVs in orthologous loci, and since it is a relatively recent endogenization/fixation, all that needs to be done is identify mechanisms that can account for that deviation. There are at least two known mechanisms to account for it (Barbulescu et al., 2001):
And the distributional NHs are not the only ERV evidence for the model of common ancestry; LTR-LTR discontinuity ratio and LTR mutation NHs are further compelling pieces. And although there is more deviation from those patterns than from those of the distribution, the fact that the patterns appear at all is powerful evidence against the parallel integration hypothesis. And the consensuses of all three patterns is downright damming to it.
this video doesn't actually prove anything, all it states is that one particular argument made by a creationist is possibly unfounded. i believe there have been many unfounded arguments made on the behalf of evolutionists in the past.
nor does it disprove anything. i don't see the slam dunk here. try again.
@ariannahiggins I don't think so, in fact, orangutans are the most distant inside the family of the great apes. Common Chimps and Bonobos are the closest.
@ariannahiggins For some reason it says that the page does not longer exist. That's fine, I will stick to the idea of chimps being our closest cousins, thanks for the information though :)
I leave my mind open for may possibilities, but how is it humans have the RH- factor in their blood, and no ape "we are related to" do not have it in their blood?
I just found that out today too about Randi. Odd how he just announced it this month publicly, yet shanedk for told of this on July 17, 2009. Surely, Shane is psychic!
It depends on how you look at it. If you go by the genetics, especially morphological changes, then they're not. We changed a LOT since we branched off.
That's crap. You are using "related" to mean "resemble". No credible biologist does that.
It might be true that [morphologically] chimps and gorillas resemble one another more than they do us, but nobody should ever confuse that with relationship to a common ancestor.
Rather than rationalize your mistake, why not simply admit it and move on.
Chiuauas have changed a lot more than German Shepards from the ancestral wolf. Is that reason enough to claim that Shepards are more closely related to the wolf than is the Chiuaua?
@kshackleton Actually, you're wrong there. German Shepherds have actually changed more BECAUSE they are more similar in morphology to wolves. They were bred BACK to that shape.
An opposum looks more like a rat than a kangaroo. Would you be foolish enough to argue that rats and 'possums are more closely related than 'possums and kangaroos?
@kshackleton "An opposum looks more like a rat than a kangaroo."
A Tasmanian wolf looks more like a dog. So what? We know from the EVIDENCE that it's not closely related: the morphology is that of a marsupial, it's generically more close to a marsupial...EVERYTHING follows the SAME nested hierarchy. How is that possible if we didn't evolve?
Yeah, I noticed that; which is why I was confused by your statement in the video that chimps are more closely related to gorillas than they are to humans. Your graph refutes your own statement.
@kshackleton We're more closely related by time, but not by genetics. The rate of evolution isn't constant; genetically, we've changed a lot more from our MRCA than chimps have.
This is simply incorrect. Genetic studies have shown that the chimp is closer, on a genetic basis, to humans that they are to gorillas. Morphological studies reach the same conclusion.
Chimps and humans are more closely related to one another than either is to the gorilla. Genetics and Morphology both support the same conclusion.
"we've changed a lot more from our MRCA than chimps have."
How does one make this determination? We have no fossils available from that time period, and none along the chimp lineage at all. We have no idea how far we great apes have diverged from our respective common ancestors.
It is true that in the coding regions responsible for things like brain development and speech, we humans have derived variants and chimps and gorillas both have more primitive variants. This is true, however, when we talk about relationships, that means our connection to common ancestry.
"Closer" in the sense of evolutionary changes. Early on in human evolution, the population dwindled to about 10,000, resulting in evolutionary changes happening faster.
The main argument against ID in my opinion is that the design is clearly not planned.
If some god is responsible for evolution then all it did was to make evolution possible and then leave it to its own devices - which is indistinguishable from there being no god and it happening on its own.
@TheRationalizer A Christian would reply that when Adam and Eve sinned (or that that account is a version of truth) the whole of creation when down the crap hole, resulting in a break down of all life and the universe itself. In my mind that is the only biblical explanation. And that is hard to believe.
@TheRationalizer I am not sure that either of your ideas would disprove a God that created by evolution, or that he allowed his creation to decay. What Shanedk said about the 100,000 years is a different kettle of fish.
@TheRationalizer I guess I would say that an all powerfull God may have reasons not known to humanity as to why he has allowed or caused these events to happen
In what way is that distinguishable from there being no god and natural selection choosing to eliminate the least suited whilst keeping any old implementation that works?
So, an all-powerful being incapable of error deliberately introduced a system which produces second class implementations of life?
It seems that people like to believe in god not only despite a lack of evidence, but also inspite of evidence to the contrary.
@shanedk I have been forced to accept that a literal reading of Genesis is most likely not possible. I would then have to accept that the Genesis account is used as a teaching tool.
@shanedk There are plenty of Christians who would support the notion that God ordained evolution. Therefore, the Genesis account is not literal. The logistics involved in Noahs flood for example, seem impossible to reconcile with science. I am just trying to be as honest as I can and throwing about some options.
@ShaneChiswick The point is, this was already settled CENTURIES ago, WAY before Darwin. The fact that we're having to go through it all again is inexcusable.
@ShaneChiswick The only problem I'd have with that is that evolution isn't goal-oriented. If he did do it, then he wasn't too picky about what he ended up with.
i'd like to see some sort of meta-study on ERV's. we can probably get a rough idea of what the odds are that such a sequence would disappear along a given line, given its current distribution. then we can compare it to our data to see what percentage of them actually did disappear, and see if they're close.
@bestvalue It´s funny, because if it did happen like you say, then Shane doesnt even need to make this debunking video. It´s the creationists who rely on the astronomical odds here in order to trye to demonstrate that we are not related to chimps and the other great apes.
Too bad you sort of missed the point of the video.
"The chances of the virus inserting itself twice in the exact same place are astronomical."
I'll give the typical evolutionist response to abiogenesis: "It must have happened because we are here."
Is what you said. Which I found to be kind of ironic, since in this case, the astronomical odds supposedly are on the creationists side - ShaneDK just shows why the odds dont matter and are not on the creationists side. But you dismiss the creationist side, even without Shane´s video
@Korkzor I guess I'll have to rewatch the video when I get time so I can make an intelligent response. It's possible that what said was in response to another comment and not to the video itself because I don't recall the content of this video.
@Korkzor Okay, I was wrong. I rewatched the video and I WAS commenting on the video. I guess I was just making a flippant remark at shanedk's mention of the astronomical odds against something happening because it is usually the evolutionists who rely heavily on the poor odds working in their favor. I figured I could play that game too. See?
@bestvalue Ye, I got what you were doing. I just found humour in the fact that you were working against yourself in this case :).. If you´ll forgive me for that.
@Korkzor Of course I would. But there's really nothing to forgive. :^D
I personally feel that it is the evolutionists who typically rely on astronomical odds - not the creationists. I think the God hypothesis is a logical deduction from the evidence. I presume you would disagree.
I wouldn't mind continuing this with you a little further since you seem like a reasonable chap (unlike many I've met on YouTube.)
I understand that, Shane, but you said that Pan and Gorilla are more "related" to each other. Without that explanation of what you meant, many people (such as myself) likely thought that you meant that Pan is more genetically related to Gorilla than to Homo.
That genus remained relatively unchanged, whereas our line suffered a population shock and dwindled to a population of about 10,000. This drove our evolution at a faster pace, causing us to change a lot more in that time.
I do have an question about evolution that someone might have an answer to.
If we look at the Gorilla-Pan-Homo branch of descent, we have 46 chromosomes while they have 48. I am aware of the chromosomal fusion and fission theory (though my ignorance is staggering) , but aren't aneuploidies usually harmful to the individual which inherits them? And if it weren't harmful to the individual, wouldn't it affect the individuals ability to mate?
The actual arrangement of chromosomes doesn't matter all that much. As long as the genes are the same. The cells should be able to pair up the original chromosomes with the fused version during fertilization. The fused chromosome becomes an allele, and genetic drift ends up selecting one or the other over time.
Could you do me, and probably a lot of others, a favor by actually defining the abbreviation ERV at the first use :) Preferably in the video description.
"but aren't aneuploidies usually harmful to the individual which inherits them"
Aneuploidies refers to having an extra copy of a chromosome or missing one. That would mean that the offspring would have 1 copy of a set of genes or 3 copies, significantly effecting trait expression.
In a fusion event, the same set of genes are still given to the offspring, even if one parent bundled them in 23 chromosomes and the other in 24. The offspring still has only 2 copies of each gene.
The point TheHeather1985 was close to making is that at the transition point between the norm being 24 pairs and the norm being 23 pairs, many zygotes would be created with aneuploidies.
There is, however, an independently determined event that would greatly ease the change in chromosome number: The Great Dieing. In this event, the population in the line that led to us dropped to something like 1000 individuals. In this small a population, drift could fix the change in chromosome number.
"wouldn't it affect the individuals ability to mate"
The viability of the offspring can be affected but does not make reproduction impossible. In fact, reduced viability can actually lead to speciation without geographic isolation as inbreeding can be more successful than breeding with the general population. The reduced gene pool variation would almost certainly force a new evolutionary strategy.
NASA scientists have discovered glycine, a fundamental building block of life, in samples of comet Wild 2 returned by NASAs Stardust spacecraft.
"Glycine is an amino acid used by living organisms to make proteins, and this is the first time an amino acid has been found in a comet,"
"Our discovery supports the theory that some of lifes ingredients formed in space and were delivered to Earth long ago by meteorite and comet impacts."
All your are showing is that evolution is unfalsifiable, everytime something hapens to be inconsisten with the tree pttern predicted by evolution, you will use this kind of excuses.
mammals do not share ervs with other classes of animals this is why we will never find an ERV in ducks chimps but not in humans.
Answerquestions1 2 weeks ago
@Answerquestions1 No, LIAR, this doesn't "happen to be inconsistent," it ISN'T INCONSISTENT!
"mammals do not share ervs with other classes of animals"
Yes they absolutely do!
"this is why we will never find an ERV in ducks chimps but not in humans."
WRONG: Evolution HAPPENED, and that's why we will never find an ERV in ducks chimps but not in humans--because it violates the nested hierarchy--but we WILL find ERVc in chimps and humans AND ducks!
shanedk 2 weeks ago
@shanedk
please show me an orthologs erv that mammals share with other classes.
btw, ervs that humans lack have been found in chimps and monkeys. so you can no longer use ´´recnt incertion´´ as an excuse (as you did in your video)
Answerquestions1 2 weeks ago
@Answerquestions1 For HUNDREDS of examples, across aves, mammals, crocodiles, and many other large-scale groups, see "Distribution of Endogenous Retroviruses in Crocodilians," Journal of Virology, 83(19): 10305-10308 (in particular, Fig. 1 on page 10306)
shanedk 2 weeks ago
@shanedk
the article does not mention any shared orthologs erv between mammals and other classes
Answerquestions1 2 weeks ago
@Answerquestions1 It most certainly does! Look at the figure I mentioned.
shanedk 2 weeks ago
@Answerquestions1 Here's another source: "Viruses and the evolution of life" by Luis P. Villarreal
From p.335: "Overall, we see evidence of lineage-specific ERV colonization in all vertebrates, well before the evolution of placental species. These early ERV colonizers are still maintained, typically in small numbers. Additionally, much more numerous and specific ERV colonization events have occurred...species lineages can be distinguished on these later ERV colonizations."
shanedk 2 weeks ago
@shanedk
he article mentions shared ervs between different classes, but they say nothing about being orthologs.
from the article:
´´The data generated here could assist future studies aimed at identifying orthologous and paralogous ERVs among crocodilians.´´
to me the quote is saying that the researchers where not even looking for orthologs ervs
Answerquestions1 2 weeks ago
Sounds like Kermit XD
iwanttocrashmybike 3 months ago
ATTENTION:(TheRationalizer) - Your feeble and immature act to block me and use of the 'F' word shows clearly YOUR inability to discourse with those who don't agree with you. Your 'threat by proxy' excuse is just 'that' - you are a coward and others on youtube should know your unfairness is ongoing! --WEAK -- ! ! ! ! ! !
hamzah938 3 months ago
0:40-0:52... caught that... i may not have the book info you have on this... but know when you insult... like so many you start with the insults first
MrAstro888 6 months ago
@MrAstro888 How is anything in that time frame an insult?
shanedk 6 months ago
lol if the predictions fails, make up an excuse and call it a coincidence hahaha
once you see tru it, this video becomes so laughable
IloveYOUviruses 1 year ago
@IloveYOUviruses The nested hierarchy and how alleles work was NOT made up after the fact to suit this! This exact scenario IS a prediction of the model!
It's the ignorance of you pathetic creationists that is laughable.
shanedk 1 year ago
@shanedk Still, this is not an explanation of differences in "ERVs" but an excuse, the only evidence that some ERVs dissapeared is that otherwise it would destroy evo "theory" (again), that only counts for the relligious deluded evo heads
IloveYOUviruses 1 year ago
@IloveYOUviruses Oh, really? Then answer this question straight:
Why would an ERV suddenly and instantly appear in every single member of the species?
shanedk 1 year ago
@shanedk Who said that ERV "appears"?? are you using the conclusion to prove the conclusion? Oh yeah, I forgot that you are the one who lied about whales evolution and Berlinsky. woah! lies and excuses plague this channel!
IloveYOUviruses 1 year ago
@IloveYOUviruses Look, IDIOT, we KNOW that ERVs appear because WE'VE SEEN IT HAPPEN! EVERY organism that gets a retrovirus (such as HIV-1, HTLV, or FLV) has the retrovirus's genome incorporated into the nucleus of the cell it attacks. That's what a retrovirus IS!!!
HOW DARE YOU accuse others of lies and excuses when YOU YOURSELF haven't even done the BASIC amount of research needed to talk about it! You creationists are the most dishonest, immoral people I ever meet!
shanedk 1 year ago
@IloveYOUviruses
“Who said that ERV "appears"?? [Are] you using the conclusion to prove the conclusion?”
The hallmark of an insertion is a displacement of chromosomal DNA, and the hallmark of insertion by integrase is the presents of target site duplication, due to the way it attacks the 5' and 3' phosphodiester bonds with an offset of a few base pairs.
MolecularBioVids2 1 year ago
Since ERVs are accompanied by target site duplications and DNA displacement, they are necessarily endogenized/fixed insertions. Combine that with their configuration of U3rU5-(pbs)-gag-pol-env-(ppt)-U3rU5, and it is undeniable that the insertions are proviral.
MolecularBioVids2 1 year ago
@MolecularBioVids2 LOOK, IF YOU WANNA IMPLY THAT ERVs ARE JUST... lol Im just kiddin, I really admire how you avoid hate-speech and name calling like that shanek guy
thanks for using real science, let me I ask to you: who says that ERVs insert at random locations?
Cuz according to Taruscio et al:
"The present results indicate that there are highly specific integration patterns for each endogenous retrovirus that do not readily relate to their sequence or particle classification..." (1991)
IloveYOUviruses 1 year ago
@IloveYOUviruses
“[Who] says that ERVs insert at random locations?”
Firstly, we know that insertion is nonspecific on the nucleotide level, due to the way it directly attacks the bonds, with no need to ligate. Yes, different retroviral integrases have biases (+/-) for an array of general genomic areas, but insertion still takes place elsewhere—just not as frequently. So, relative to pure randomness, insertion is highly specific, but relative to locus specificity, insertion is highly random.
MolecularBioVids2 1 year ago
This is also pointed out in the Taruscio (1991) paper:
"Retroviruses have the ability to integrate into the genome of their host, in many cases with little apparent sequence or site specificity. However, relatively few studies have addressed more general features of chromosomal integration... These investigators have suggested that higher order structural features, or an active transcriptional capacity of chromatin may be fundamental for preferred integration events (p.141-142)."
MolecularBioVids2 1 year ago
The number of species that share ERVs in orthologous loci requires downright locus specificity on the nucleotide level for the observed sharing to occur via separate insertion in distinct lineages. Given this requirement, and given the large number of species (all primates, for instance) that share ERVs in orthologous loci (Anderssen et al., 1997), the model of uncommon ancestry is falsified and inheritance from a common ancestral species is necessitated.
MolecularBioVids2 1 year ago
Secondly, even if insertion were locus specific, the only way that the hierarchical sets could arise is if infection susceptibility varied precisely with genetic commonality and if all species were infected, regardless of geographic isolation. Not only does the observed distribution of ERVs show this not the case (Polavarapu, Bowen, & McDonald, 2006; Yohn et al., 2005), but the restriction capability of the innate immune system also shows no such pattern (Kaiser, Malik, and Emerman, 2006).
MolecularBioVids2 1 year ago
@MolecularBioVids2 Taruscio et. al noticed that there was little research on that topic (integration preference) so they estudied 3 kinds of ERVs and realizad that "Each retroviral sequence exhibited a unique and markedly different integration pattern.", *IF* there is preference for integration, the NH argument is pointless, maybe nothing more than a good circular guess.
Please, tell me if Taruscio was wrong back at the 90's, did he lied? Is he just an amateur? What happened?
IloveYOUviruses 1 year ago
@IloveYOUviruses if we can't get over a paper from 1991 it would be pointless to touch the more recent topic of the thousands of (somehow) very useful ERVs.
IloveYOUviruses 1 year ago
@IloveYOUviruses
“[If] we can't get over a paper from 1991 it would be pointless to touch the more recent topic of the thousands of (somehow) very useful ERVs.”
There are no truly functional ERVs; there are only functional components.
MolecularBioVids2 1 year ago
@MolecularBioVids2 "Because there are 50-1000 copies of each of these retroviruses in the genome, it was possible to evaluate repeated integration events. Each retroviral sequence exhibited a unique and markedly different integration pattern... The present results indicate that there are highly specific integration patterns for each endogenous retrovirus that do not readily relate to their sequence or particle classification."
How much can you twist Taruscio study?
IloveYOUviruses 1 year ago
@IloveYOUviruses
“How much can you twist Taruscio study?”
I have not twisted it at all. Please read and what I said again. Once again, the preference reported in the Taruscio study is for the general proximity of “higher order structural features;” not between specific base pairs (loci). Insertion was known to be nonspecific on the nucleotide level then, and subsequent study has confirmed this, as well as confirmed the high order preference. This does not explain ERVs shared at specific loci.
MolecularBioVids2 11 months ago
@MolecularBioVids2 Mitchell didn't refuted Taruscio, he worked with other ERVs and proved that some ERVs can be more biased than others, besides, Mitchel's team used strains derived from pathogenic viruses wich are known to be dangerous (obviously!) unlike the thousands of (somehow) very useful ERVs... which reminds me...
IloveYOUviruses 1 year ago
@IloveYOUviruses
“Mitchell didn't [refute] Taruscio, he worked with other ERVs and proved that some ERVs can be more biased than others...”
Firstly, I explicitly stated that The Mitchell study corroborated the Taruscio study. Secondly, the Mitchell study showed not only different levels of bias, but also entirely different biases; and I never contradicted what you just said.
MolecularBioVids2 11 months ago
“...besides, [Mitchell's] team used strains derived from pathogenic viruses [which] are known to be dangerous (obviously!) unlike the thousands of (somehow) very useful ERVs...”
As I already explained, components of proviruses are sometimes co-opted, and the remainder left to mutate to the point that they lack virulence. And the Mitchell study was mealy an assessment of the operation of viral integrase. Arguing about virulence is a non sequitur.
MolecularBioVids2 11 months ago
@MolecularBioVids2 ...that you seem to be confused, I never said ERVs were totally useful, we don't know that, neither we know that "There are no truly functional ERVs" or "there are only functional components.", that would be the same error as those who said that 95% of the DNA was junk and then one guy discovered it wasn't, patented it and got disgustingly rich, this kind of reasoning has always been detrimental to science, be careful.
IloveYOUviruses 1 year ago
@IloveYOUviruses
“...I never said ERVs were totally [useful;] we don't know [that;] neither [do] we know that ‘There are no truly functional ERVs’ or ‘there are only functional components...’”
By ‘none’ and “only,” I am strictly referencing the data collected thus far. All current observations indicate what I said. These data indicate exaptation and scaffolding. Thus my point still stands that “functionality is simply a red herring, when discussing how ERVs necessitate common ancestry.”
MolecularBioVids2 11 months ago
@MolecularBioVids2 gotta go, I was keeping this for the end:
Retroviral promoters in the human genome
Andrew B. Conley
They show that ERVs are involved in the transcription on 1/5th of the genome, that's way too much for a random insertion and clearly shows a pattern
And about targeting sequences, that's a well documented topic, and I admit, the bias depends of the ERV
with all that info, ERVs+NH is just a good circular hope
IloveYOUviruses 1 year ago
@IloveYOUviruses Even if this phantom "pattern" of yours actually existed, that would still mean that a retrovirus would have AT BEST a 1 in 600,000,000 chance of inserting itself at a particular location in the human genome. Doesn't help you.
shanedk 1 year ago
@IloveYOUviruses
“[A. B. Conley et al.] show that ERVs are involved in the transcription on 1/5th of the genome, that's way too much for a random insertion and clearly shows a pattern.”
As stated in the Conley study, “approximately 5% of the human genome sequence is derived from retroviruses (p.1563).” The reference they give is the ‘Initial sequencing and analysis of the human genome’ paper, which states that 2.03×10^5 class I/II/III ERVs comprise 4.64% the human genome (Lander et al., 2001).
MolecularBioVids2 11 months ago
The “51,197 ERV-derived promoter sequences that initiate transcription within the human genome (Conley, 2008, p.1563)” represent only 25.2% of total insertions. Add to that leaky transcription, and the fact that truly beneficial insertions can subsequently be subjected to directional selection, and the observation that “PET tags that capture transcripts initiated from ERVs cover 22.4% of the genome (p.1566)” doesn’t contradict observations of nonspecific nucleotide level insertion.
MolecularBioVids2 11 months ago
“And about targeting sequences, that's a well documented topic, and I admit, the bias depends [on] the ERV. [With] all that info, ERVs+NH is just a good circular hope.”
I’ve already explained how none of this indicates locus specificity. But you need to understand that even if it did, it doesn’t even begin to explain the hierarchical grouping of shared ERVs. For the third time:
MolecularBioVids2 11 months ago
Even if insertion were locus specific, the only way the shared ERVs could be hierarchically grouped, and also the result of parallel integration, is if infection susceptibility to vary precisely with genetic commonality, and for precise species-wide infection, regardless of geographic isolation.
MolecularBioVids2 11 months ago
The observed distribution of ERVs and the observed variation in restriction capability of the innate immune system each result in no such grouping; thus they falsify the parallel integration hypothesis.
MolecularBioVids2 11 months ago
Another thing that the parallel integration hypothesis utterly fails to explain is the positive correlation between number of species that share orthologous ERVs and the discontinuity between the 5’ and 3’ LTRs of those ERVs. It also doesn’t explain the sharing of mutations between orthologous ERVs’ LTRs, the hierarchical grouping of such mutations, or that the nested hierarchies of distribution match those of mutation.
MolecularBioVids2 11 months ago
All of these observed data are necessitated by the evolutionary model, yet falsify the parallel integration hypothesis.
MolecularBioVids2 11 months ago
Examples include viral LTRs replacing or augmenting a gene’s preexisting promoters (Cohen, Lock, & Mager, 2009), or enJSRV env and gag genes contributing to placental growth/differentiation regulation (Dunlap et al., 2006; Palmarini et al., 2000) and causing gag-gag interaction that restrict pathogenic JSRVs (Mura et al., 2004), respectively. There are also very few ERVs that are even in a configuration and/or position that they can contribute any function.
MolecularBioVids2 1 year ago
That it is only a few functional components from a small percentage of ERVs is not only positive evidence that the functions were co-opted, rather than designed in, but it falsifies the idea that ERVs exist solely to benefit the host organisms, that ERVs were designed in genomes from the beginning, and that shared ERVs must be designed there to confer a similar benefit.
MolecularBioVids2 1 year ago
But it gets worse; even this evidence is a moot point, because we know that ERVs are proviral insertions that have been endogenized and fixed in populations. We know this due to their sequences and due to the presence of DNA displacement and target site duplication. [refer to the first two posts I made to you for a detailed explanation]
MolecularBioVids2 1 year ago
This more than falsifies the idea that ERVs were designed in, since the fact that they are insertion means that there was a time when the organism existed in some form without them, prior to their insertion.
Any functional components are necessarily post-insertion exaptations, and the fact that they are necessarily insertion means that they can not be part of any 'original design.' The issue of functionality is simply a red herring, when discussing how ERVs necessitate common ancestry.
MolecularBioVids2 1 year ago
@IloveYOUviruses Oh, come on--in 1991 they didn't even know enough to make the antiretroviral drugs we have today that have stopped making AIDS the death sentence it once was! They barely had transcriptase inhibitors. A LOT has been learned since then. 20 years is a LONG time in science.
shanedk 1 year ago
@IloveYOUviruses
“Taruscio et. al noticed that there was little research on that topic (integration preference) so they [studied] 3 kinds of ERVs and [realized] that ‘Each retroviral sequence exhibited a unique and markedly different integration pattern.’... Please, tell me if Taruscio was wrong back at the 90's, did he [lie?] Is he just an amateur?”
Dr. Taruscio was correct, and continued research over the past couple decades confirms her findings. But you are misunderstanding these findings:
MolecularBioVids2 1 year ago
The ‘preferences’ are merely minor statistical biases for or against insertion within the very general areas of “chromosomal regions rich in expressed genes… [their interwoven] CpG islands… active genes… [and areas] near transcription start sites (Mitchell et al., 2004),” but these biases are so minor, that they require thousands of trials (3127 used in the Mitchell study) just to detect them. And insertion still occurs out of the preferred areas—just with decreased frequency.
MolecularBioVids2 1 year ago
And that is merely the “higher order structural” level—it remains true that insertion is nonspecific on the nucleotide level. When Dr. Taruscio says “unique and markedly different integration [patterns],” she is referencing the distinct differences in the deviation from randomness. And again the findings are consistent with the fact that, relative to pure randomness, insertion is highly specific, but relative to locus specificity (nucleotide level), insertion is highly random.
MolecularBioVids2 1 year ago
“*IF* there is preference for integration, the NH argument is pointless, maybe nothing more than a good circular guess.”
That is quite inaccurate. Again, the number of species that share ERVs requires locus specificity, for the observed sharing to occur via parallel integration. The preferences are nowhere near that. Thus the large number of species that share ERVs falsify the parallel integration hypothesis, and necessitate common ancestral species.
MolecularBioVids2 1 year ago
And (also) again, even if insertion were locus specific, parallel integration requires infection susceptibility to vary precisely with genetic commonality, and for precise species-wide infection, regardless of geographic isolation.
The observed distribution of ERVs and the observed variation in restriction capability of the innate immune system each falsify the parallel integration hypothesis.
MolecularBioVids2 1 year ago
@IloveYOUviruses
“Still, this is not an explanation of differences in ‘ERVs’ but an excuse, the only evidence that some ERVs [disappeared] is that otherwise it would destroy evo ‘theory’ (again), that only counts for the [religious] deluded evo heads.”
You are not thinking analytically. I’ll explain:
MolecularBioVids2 1 year ago
Although patterns are formed and act as powerful evidence of past occurrences and of mechanisms that causes them, the complex nature of the physical world (due to so many simultaneous interactions on so many levels) often causes deviation from those patterns.
Thus the patterns act as indicators of what is actually going on, and deviation from them is both expected and rendered likely not indicative of what is actually going on.
MolecularBioVids2 1 year ago
Since HERV-K-GC1 is the only known deviation from the distributional nested hierarchy of ERVs in orthologous loci, and since it is a relatively recent endogenization/fixation, all that needs to be done is identify mechanisms that can account for that deviation. There are at least two known mechanisms to account for it (Barbulescu et al., 2001):
MolecularBioVids2 1 year ago
1) allelic segregation – insertion in an allele that remained heterozygous in the populations across two divergences (most parsimonious)
2) insertion in a duplicate section of the chromosome that underwent homologous recombination in each respective linage
MolecularBioVids2 1 year ago
And the distributional NHs are not the only ERV evidence for the model of common ancestry; LTR-LTR discontinuity ratio and LTR mutation NHs are further compelling pieces. And although there is more deviation from those patterns than from those of the distribution, the fact that the patterns appear at all is powerful evidence against the parallel integration hypothesis. And the consensuses of all three patterns is downright damming to it.
MolecularBioVids2 1 year ago
this video doesn't actually prove anything, all it states is that one particular argument made by a creationist is possibly unfounded. i believe there have been many unfounded arguments made on the behalf of evolutionists in the past.
nor does it disprove anything. i don't see the slam dunk here. try again.
ferrel81 1 year ago
Are LTRs always the same length for a given virus, or are they random within a range?
Also, does this vary per virus or is the same answer common to all retroviruses?
TheRationalizer 1 year ago
Using James Randi's photo with the word "Homo" written above it, was that a pun? :)
TheRationalizer 1 year ago
@TheRationalizer No, he hadn't come out yet at the time I made this video. It's just a coincidence.
shanedk 1 year ago
@shanedk
A funny coincidence, one I think he'd laugh at :D
TheRationalizer 1 year ago
I read there's a new theory that orangutans may actually be the closest relation to us...based on a finding, and mophological analysis
ariannahiggins 1 year ago
@ariannahiggins I don't think so, in fact, orangutans are the most distant inside the family of the great apes. Common Chimps and Bonobos are the closest.
JUANMO94 1 year ago
@JUANMO94 Yes I know chimps and bonobos are, but there was some new piece of evidence which disagreed with that idea....oh here I found it
w w w .sciencedaily. com/releases/2009/06/090618084304. htm
ariannahiggins 1 year ago
@ariannahiggins For some reason it says that the page does not longer exist. That's fine, I will stick to the idea of chimps being our closest cousins, thanks for the information though :)
JUANMO94 1 year ago
@JUANMO94 um, I think you have to delete the spaces.
ariannahiggins 1 year ago
@ariannahiggins I did
JUANMO94 1 year ago
morphological similarity is not the be-all end-all, the best evidence is when genetic info and morphological info coincide
ariannahiggins 1 year ago
awesome explanation.
ariannahiggins 1 year ago
I leave my mind open for may possibilities, but how is it humans have the RH- factor in their blood, and no ape "we are related to" do not have it in their blood?
LutzfromPS2 1 year ago
@LutzfromPS2 The RH-negative allele has been traced back to 35,000 years ago, LONG after our divergence from the line that led to chimpanzees.
shanedk 1 year ago
This comment has received too many negative votes show
evolution is just a religion
blue33sky 1 year ago
@blue33sky Mmmh, nope, you are wrong there. Evolution is a scientific theory.
JUANMO94 1 year ago
I didn't know that Randy was a homo.
deerfieldproductions 2 years ago 2
I just found that out today too about Randi. Odd how he just announced it this month publicly, yet shanedk for told of this on July 17, 2009. Surely, Shane is psychic!
MrBiological 1 year ago 3
@deerfieldproductions
He is, really. He came out a while back.
TheRationalizer 1 year ago
I should add that it was an excellent video and I was prepared to give you 5 stars until I heard that final statement.
kshackleton 2 years ago
Chimps and bonobos are more closely related to humans than they are to gorillas, as indicated by your diagram.
kshackleton 2 years ago 2
It depends on how you look at it. If you go by the genetics, especially morphological changes, then they're not. We changed a LOT since we branched off.
In terms of time, you're right.
shanedk 2 years ago
@shanedk
The term "related" is generally understood by the people who watch the videos [and biologists] to refer to relationship to a common ancestor.
To claim that we are more distantly related because some of our traits are more derived is more than misleading, it's incorrect usage of the term.
kshackleton 2 years ago
It's the way a lot of biologists use the term.
shanedk 2 years ago
@shanedk
That's crap. You are using "related" to mean "resemble". No credible biologist does that.
It might be true that [morphologically] chimps and gorillas resemble one another more than they do us, but nobody should ever confuse that with relationship to a common ancestor.
Rather than rationalize your mistake, why not simply admit it and move on.
kshackleton 2 years ago
It's NOT a mistake. Look up "genetic distance."
shanedk 2 years ago
@shanedk
Analysis of genetic distance is rather consistent in supporting a Human-Pan clade rather than a Pan-Gorilla clade.
Anyway, it's irrelevant to your inference that biologists interchange "resemble" with "related".
The amount of derivation from the common ancestor has no impact on relatedness.
kshackleton 2 years ago 2
Your closing statement is incorrect and is refuted by your own diagram.
Chimps and Bonobos diverged from a common ancestor perhaps 3 million years ago.
Humans, Chimps, and Bonobos all share a common ancestor which lived perhaps 6 to 7 million years ago.
Humans, Chimps, Gorillas, and Bonobos share a common ancestor which lived some 10 or so million years ago.
kshackleton 2 years ago
Yes, but again we've changed a lot more during that time than they have.
shanedk 2 years ago
@shanedk
Chiuauas have changed a lot more than German Shepards from the ancestral wolf. Is that reason enough to claim that Shepards are more closely related to the wolf than is the Chiuaua?
kshackleton 2 years ago 2
@kshackleton Actually, you're wrong there. German Shepherds have actually changed more BECAUSE they are more similar in morphology to wolves. They were bred BACK to that shape.
evensgrey 1 year ago
@evensgrey
And how does that affect relatedness?
An opposum looks more like a rat than a kangaroo. Would you be foolish enough to argue that rats and 'possums are more closely related than 'possums and kangaroos?
kshackleton 1 year ago
@kshackleton "An opposum looks more like a rat than a kangaroo."
A Tasmanian wolf looks more like a dog. So what? We know from the EVIDENCE that it's not closely related: the morphology is that of a marsupial, it's generically more close to a marsupial...EVERYTHING follows the SAME nested hierarchy. How is that possible if we didn't evolve?
shanedk 1 year ago
@shanedk
You should learn to read upthread before replying.
kshackleton 1 year ago
@kshackleton I read the entire thread. I followed it as it was being posted. Stop making excuses; you're WRONG.
shanedk 1 year ago
@shanedk
You seem to think that I do not accept evolution...I do.
kshackleton 1 year ago
@shanedk
I also accept the nested hierarchy and the evidence of ERV's as compelling evidence of the common ancestry of life.
What I find odd is why you believe that chimps, bonobos, and gorillas should be grouped together and humans be the outlier?
kshackleton 1 year ago
@kshackleton Um, I didn't. Check the graph again.
shanedk 1 year ago
@shanedk
Yeah, I noticed that; which is why I was confused by your statement in the video that chimps are more closely related to gorillas than they are to humans. Your graph refutes your own statement.
kshackleton 1 year ago
@kshackleton We're more closely related by time, but not by genetics. The rate of evolution isn't constant; genetically, we've changed a lot more from our MRCA than chimps have.
shanedk 1 year ago
@shanedk
This is simply incorrect. Genetic studies have shown that the chimp is closer, on a genetic basis, to humans that they are to gorillas. Morphological studies reach the same conclusion.
Chimps and humans are more closely related to one another than either is to the gorilla. Genetics and Morphology both support the same conclusion.
kshackleton 1 year ago
@shanedk
"we've changed a lot more from our MRCA than chimps have."
How does one make this determination? We have no fossils available from that time period, and none along the chimp lineage at all. We have no idea how far we great apes have diverged from our respective common ancestors.
kshackleton 1 year ago
@kshackleton This, BTW, is why they don't use coding DNA to determine evolutionary timelines. They use things like mtDNA, junk DNA, and ERVs.
shanedk 1 year ago
@shanedk
Yes, I understand that. It's how the relationships are determined.
kshackleton 1 year ago
@shanedk
I think that I see where you are going now.
It is true that in the coding regions responsible for things like brain development and speech, we humans have derived variants and chimps and gorillas both have more primitive variants. This is true, however, when we talk about relationships, that means our connection to common ancestry.
kshackleton 1 year ago
And here I thought all the made up science about genetic memories from Assassin's Creed was confusing. Real science makes me mind spin.
GumbaMasta 2 years ago
Thanks Shane, great vid
dlandon2000 2 years ago
Chimps, Bonobos and Gorillas are more closely related to each other than to humans?
Hm, weird. I thought I once heard someone say chimps are closer to humans than they are to Bonobos..
Mithcoriel 2 years ago
"Closer" in the sense of evolutionary changes. Early on in human evolution, the population dwindled to about 10,000, resulting in evolutionary changes happening faster.
shanedk 2 years ago
Very nice! I think even I understood that :) Very clear and well-resented.
OMG, my IQ just dropped 6 points from posting a comment on youtube! No, rly!
susanhogarth 2 years ago
Grr. Well-Presented, not Resented!
My "P" key is acting up!
susanhogarth 2 years ago
I used the wrong word...I meant I would be devistated from an ID position.
ShaneChiswick 2 years ago
Shane I am a Christian who is studying evolution. if the evidence of ERV is true it would be astonishing for ID.
What argument could you make against the evidence and accuracy of ERV
ShaneChiswick 2 years ago
How on EARTH is this a win for ID???
shanedk 2 years ago
@ShaneChiswick
The main argument against ID in my opinion is that the design is clearly not planned.
If some god is responsible for evolution then all it did was to make evolution possible and then leave it to its own devices - which is indistinguishable from there being no god and it happening on its own.
TheRationalizer 1 year ago
Comment removed
ShaneChiswick 1 year ago
@ShaneChiswick And then they suddenly got separated by 100,000 years???
shanedk 1 year ago
@shanedk what do u mean?
Sorry about my spelling and grammar before, I need to give myself an uppercut.
ShaneChiswick 1 year ago
@ShaneChiswick That's the difference in time span between Y-Nuclear Adam and Mitochondrial Eve. I have a video on the subject.
shanedk 1 year ago
@TheRationalizer A Christian would reply that when Adam and Eve sinned (or that that account is a version of truth) the whole of creation when down the crap hole, resulting in a break down of all life and the universe itself. In my mind that is the only biblical explanation. And that is hard to believe.
ShaneChiswick 1 year ago
@ShaneChiswick
Which means that either
A: God created a design capable of becoming imperfect, which is imperfect of God.
B: Man is so powerful we can somehow alter the design of God, which disproves omnipotentcy
TheRationalizer 1 year ago
@TheRationalizer I am not sure that either of your ideas would disprove a God that created by evolution, or that he allowed his creation to decay. What Shanedk said about the 100,000 years is a different kettle of fish.
ShaneChiswick 1 year ago
@ShaneChiswick
No, neither would disprove "creator god", although evolution does disprove torah god, bible god, Islam god, and all other derivatives.
However, what it would disprove is a perfect + all powerful god.
TheRationalizer 1 year ago
@TheRationalizer I guess I would say that an all powerfull God may have reasons not known to humanity as to why he has allowed or caused these events to happen
ShaneChiswick 1 year ago
@ShaneChiswick
In what way is that distinguishable from there being no god and natural selection choosing to eliminate the least suited whilst keeping any old implementation that works?
So, an all-powerful being incapable of error deliberately introduced a system which produces second class implementations of life?
It seems that people like to believe in god not only despite a lack of evidence, but also inspite of evidence to the contrary.
TheRationalizer 1 year ago
@ShaneChiswick That's a disproof of a literal reading of Genesis, something that has been soundly torn apart by science numerous ways.
shanedk 1 year ago
@shanedk I have been forced to accept that a literal reading of Genesis is most likely not possible. I would then have to accept that the Genesis account is used as a teaching tool.
ShaneChiswick 1 year ago
@ShaneChiswick Great; you've reached the level of Thomas Aquinas. Welcome to the 13th Century...
shanedk 1 year ago
@shanedk There are plenty of Christians who would support the notion that God ordained evolution. Therefore, the Genesis account is not literal. The logistics involved in Noahs flood for example, seem impossible to reconcile with science. I am just trying to be as honest as I can and throwing about some options.
ShaneChiswick 1 year ago
@ShaneChiswick The point is, this was already settled CENTURIES ago, WAY before Darwin. The fact that we're having to go through it all again is inexcusable.
shanedk 1 year ago
@shanedk What problem would u have with a God who chooses to use evolution so that it was certain man would arrive?
ShaneChiswick 1 year ago
@ShaneChiswick The only problem I'd have with that is that evolution isn't goal-oriented. If he did do it, then he wasn't too picky about what he ended up with.
shanedk 1 year ago
@shanedk your lie peddling is inexcusable
ferrel81 1 year ago
@ferrel81 That's not a lie; that's an easily-verifiable fact, and if you'd bother to just look it up you'd see that.
shanedk 1 year ago
@ferrel81
Projection for the win. :P
vspqbd 1 year ago
i'd like to see some sort of meta-study on ERV's. we can probably get a rough idea of what the odds are that such a sequence would disappear along a given line, given its current distribution. then we can compare it to our data to see what percentage of them actually did disappear, and see if they're close.
ATL45 2 years ago
I would think that the equations from genetic drift would satisfy that.
shanedk 2 years ago
Out of interest, do you know if any of your subs are creationists?
DanJC989 2 years ago
No idea.
shanedk 2 years ago
I have a half-attached earlobe. A better argument would be hermaphrodite.
Scoforever 2 years ago
In what way is it "half-attached"?
shanedk 2 years ago
I might get a video of it to show you. It's basically at a 90 degree angle to my head.
Scoforever 2 years ago
That's considered attached.
shanedk 2 years ago
"The chances of the virus inserting itself twice in the exact same place are astronomical."
I'll give the typical evolutionist response to abiogenesis: "It must have happened because we are here."
bestvalue 2 years ago
Um, that is NOT the "evolutionist" response.
My upcoming book has a lengthy appendix on abiogenesis.
shanedk 2 years ago
Upcoming book?
Please keep us posted.
Leehofooks 2 years ago
It's a companion book to "How Evolution Is Scientific," which will coincide with the Second Edition of the DVD/Blu-Ray disc.
shanedk 2 years ago
@bestvalue It´s funny, because if it did happen like you say, then Shane doesnt even need to make this debunking video. It´s the creationists who rely on the astronomical odds here in order to trye to demonstrate that we are not related to chimps and the other great apes.
Too bad you sort of missed the point of the video.
Korkzor 1 year ago
@Korkzor Sorry, Kork, but it's apparently been 11 months since I posted on this video. Can you refresh my memory as to what you're talking about?
bestvalue 1 year ago
@bestvalue
"The chances of the virus inserting itself twice in the exact same place are astronomical."
I'll give the typical evolutionist response to abiogenesis: "It must have happened because we are here."
Is what you said. Which I found to be kind of ironic, since in this case, the astronomical odds supposedly are on the creationists side - ShaneDK just shows why the odds dont matter and are not on the creationists side. But you dismiss the creationist side, even without Shane´s video
Korkzor 1 year ago
@Korkzor I guess I'll have to rewatch the video when I get time so I can make an intelligent response. It's possible that what said was in response to another comment and not to the video itself because I don't recall the content of this video.
bestvalue 1 year ago
@Korkzor Okay, I was wrong. I rewatched the video and I WAS commenting on the video. I guess I was just making a flippant remark at shanedk's mention of the astronomical odds against something happening because it is usually the evolutionists who rely heavily on the poor odds working in their favor. I figured I could play that game too. See?
bestvalue 1 year ago
@bestvalue Ye, I got what you were doing. I just found humour in the fact that you were working against yourself in this case :).. If you´ll forgive me for that.
Korkzor 1 year ago
@Korkzor Of course I would. But there's really nothing to forgive. :^D
I personally feel that it is the evolutionists who typically rely on astronomical odds - not the creationists. I think the God hypothesis is a logical deduction from the evidence. I presume you would disagree.
I wouldn't mind continuing this with you a little further since you seem like a reasonable chap (unlike many I've met on YouTube.)
bestvalue 1 year ago
I understand that, Shane, but you said that Pan and Gorilla are more "related" to each other. Without that explanation of what you meant, many people (such as myself) likely thought that you meant that Pan is more genetically related to Gorilla than to Homo.
SaimDI 2 years ago
I may have misinterpreted what you said but:
'Chimpanzees, gorillas and bonobos are more related to each other than to humans'
The Pan genus is more related to the Homo genus than to the Gorilla genus.
SaimDI 2 years ago
That genus remained relatively unchanged, whereas our line suffered a population shock and dwindled to a population of about 10,000. This drove our evolution at a faster pace, causing us to change a lot more in that time.
shanedk 2 years ago
LOL because it says "homo" over james randi
macman13 2 years ago
Why does it make you laugh that there's a derivative of the old latin word for "human" above James Randi?
shanedk 2 years ago
Same reason it would make me laugh if there were an antiquated term for "happy or carefree" over his picture.
macman13 2 years ago 2
I do have an question about evolution that someone might have an answer to.
If we look at the Gorilla-Pan-Homo branch of descent, we have 46 chromosomes while they have 48. I am aware of the chromosomal fusion and fission theory (though my ignorance is staggering) , but aren't aneuploidies usually harmful to the individual which inherits them? And if it weren't harmful to the individual, wouldn't it affect the individuals ability to mate?
P.S. I am NOT a creationist, no ad hominems.
TheHeather1985 2 years ago
The actual arrangement of chromosomes doesn't matter all that much. As long as the genes are the same. The cells should be able to pair up the original chromosomes with the fused version during fertilization. The fused chromosome becomes an allele, and genetic drift ends up selecting one or the other over time.
shanedk 2 years ago
Could you do me, and probably a lot of others, a favor by actually defining the abbreviation ERV at the first use :) Preferably in the video description.
Nerusai 2 years ago
Oops, I should have done that, huh?
shanedk 2 years ago
"but aren't aneuploidies usually harmful to the individual which inherits them"
Aneuploidies refers to having an extra copy of a chromosome or missing one. That would mean that the offspring would have 1 copy of a set of genes or 3 copies, significantly effecting trait expression.
In a fusion event, the same set of genes are still given to the offspring, even if one parent bundled them in 23 chromosomes and the other in 24. The offspring still has only 2 copies of each gene.
zebraone100 2 years ago
The point TheHeather1985 was close to making is that at the transition point between the norm being 24 pairs and the norm being 23 pairs, many zygotes would be created with aneuploidies.
There is, however, an independently determined event that would greatly ease the change in chromosome number: The Great Dieing. In this event, the population in the line that led to us dropped to something like 1000 individuals. In this small a population, drift could fix the change in chromosome number.
evensgrey 2 years ago
(cont.)
"wouldn't it affect the individuals ability to mate"
The viability of the offspring can be affected but does not make reproduction impossible. In fact, reduced viability can actually lead to speciation without geographic isolation as inbreeding can be more successful than breeding with the general population. The reduced gene pool variation would almost certainly force a new evolutionary strategy.
zebraone100 2 years ago
lol I must confess that I obviously didn't undertsand ERVs either; we're only at the 3:13 mark and I've just went "Oh..."
I must admit I had thought the same as most Creationists: ERVs are passed down regardless. Oops. :p
AnimaRaptor 2 years ago
August 17, 2009
NASA scientists have discovered glycine, a fundamental building block of life, in samples of comet Wild 2 returned by NASAs Stardust spacecraft.
"Glycine is an amino acid used by living organisms to make proteins, and this is the first time an amino acid has been found in a comet,"
"Our discovery supports the theory that some of lifes ingredients formed in space and were delivered to Earth long ago by meteorite and comet impacts."
astrobiology(dot)nasa(dot)gov
LuskinsConscience 2 years ago
And it's far from the first one. Those organic molecules are everywhere!
shanedk 2 years ago
(Also, FYI, I have Googled, but my lack of academic access to PRVs at the moment means I can't actually read most of what I'm finding.)
mathlaura 2 years ago
I am a dumbass and posted the addendum to my comment on the wrong video. Disregard!
mathlaura 2 years ago