 Such that if you let the engine of evolution run, random variation being acted on by natural selection, genuine novelty will arise that you could not have anticipated on the basis of your starting population. In other words, the variation we see of populations today, whether induced by us, by newgins or artificial methods, but also natural populations, represents the raw materials for evolution at all scales, from the micro right on off to the macro. That's the argument. Now, what's happened in the past 30 years is that has been shown to be false. Not because, you know, some crazy person like me in intelligent design theorists was determined that it was going to be false. That's not actually my view, but it was shown by research within the neo-Germany framework itself to be false. And one of the first ways that this was discovered was by developmental biologists, reverse engineering model systems like the SOCLA to figure out how they developed. So I was a student freshman studying biology at the University of Pittsburgh when this paper was published. And I remember the excitement surrounding the paper, because for the first time, using a technique called saturation mutagenesis, as the European Black in the Biology Laboratory in Heidelberg, Christiana Hussain-Bullhardt and her collaborator, Eric Wieskusen, figured out some of the steps involved in how a poop fly was built. And they ended up winning the Nobel Prize in medicine in 1995 for their work. And what they did was really, in many ways, a kind of reverse engineering. Using mutagens, they disrupted genes against their protein products, and they watched what happened to the developmental anatomy of fruit flies as those genes and their protein products were disrupted. So here is our starting point, the fertilized egg of a fruit fly. And these genes that they disrupted at various points along this trajectory, as this single cell expands to the millions of cells that we find in the adult fly here, there are downstream consequences that follow from those mutations, and those consequences are increasingly severe the earlier the mutations occur. You can see why, because there's a causal asymmetry in the developmental process. Think about it this way. You want to visit a friend in Austin, where you've newly moved here to Dallas. You don't actually know where Austin is. Your knowledge of Texas geography is abysmal. And you go on the site and you think it's a map quest. In fact, some hacker has put up a perverse map quest, and the first direction you get in your map quest series of steps is to go north. Now, if nothing ever corrects that, you'll find yourself at some point Oklahoma, or farther north. You're not any closer to Austin than you were when you left your driveway because your first step was wrong. As a consequence, unless you correct that first wrong step, everything that's in its train is going to be wrong as well. Well, to take that analogy back into development of biology, if these early steps don't function properly in development, everything downstream of them will be in trouble. So that's what they did. And what they found was remarkable. Now, this picture shows in the left-hand column the normal phenotype, the normal form of a fruit fly larva. That's what it normally looks like, but hasn't developed enough. These pictures on the right-hand columns are the mutant forms, and they're all dead. They're not going anywhere because in the process of their development, key embryonic regulators have been disrupted so that the downstream consequences are overwhelming and egalitarian to the embryo. In fact, the embryos are dead. Well, you can see that you can figure out how the normal system works. If you disrupt it over and over and over, you can see what genes and proteins are necessary for normal development. The consequence, though, is you discover you're killing a lot of flies. It's not hard to understand why, and there's no mystery here. It's just because development has this causally asymmetric structure, where these early events are critical to what follows. Now, let's take this knowledge, which was generated by really thoroughly Germanic sort of unbelievably ruthless and detailed experiments with well-deserving of a Nobel Prize, and apply it to the problem of evolution, of macroevolution. This picture shows you, by the way, the developmental cascaded mesophila as it normally unfolds, and you've got your starting point here. This is a single cell at this point. There aren't even any cell membranes except for the outside one, and there's a chain of events that, under normal circumstances, will give you the larva, which will then, of course, later on develop into the adult fly. So remember any other slide from my little talk tonight. Remember this one. Here's the problem in three fundamental steps. Animals. Animal body planes are normally built by starting with a single cell of fertilized egg, which, depending on the species in question, will then divide and divide and divide giving you the adult form where you can start the process over again. That's how it works. If you want to change the global form, the architecture of that animal, you've all been into something else. You've got to start at the beginning because that's where the body plan is put in place. And we know this not just from jisophila, but from lots of other models, like sea urchins, mice, frogs, and so forth. Put those two together and you have an insoluble problem for neodermal human theory because mutations that occur early that affect body plan formation are overwhelmingly destructive to the organism and the way they are being expressed. This is the clear signal that has come back to biologists from fruit flies since Morgan's fly room in Columbia 110 years ago. If you want a viable fly, it can reproduce. You better have those early stages functioning correctly. And I think that that is not overstating the problem. This is a fundamental difficulty in this area of theory. If we go back now and look at the Cambrian explosion, the same difficulty arises because if more bilateria existed, there were probably on the order of hundreds of thousands, if not more, cells in that creature. Those cells are specified to particular functional roles, their guts, their skin, sense organs, and so forth. There's going to be a developmental process building back too. If we're going to change the form of this and evolve it into something else, we're going to have to disrupt this development and the same problem recurs. There's no reason to think that this logic can be violated in the Cambrian any more than it can today. This is not a secret. This is not a secret. This problem is well-known in evolutionary theory. When I was a student, now at this point, I was a junior at studying evolutionary biology. I read a really fine paper by John McDonald, his geneticist at Georgia Tech, and he said these kinds of patterns point to what he called the great Darwinian paradox, and here's how he put it in the very next sentence. I'll translate this for you because we're running short of time. Genes and organisms that vary discernibly, we can see variations occurring in those genes. That's what he means by loci here. Do not seem to lie at the basis of major adaptive change, like building a body. Those genes do not vary because if they did, the organism wouldn't know where it was going in the developmental process. They're apparently not variable. David to Caltech has been trying to solve this problem in his own research, and he says, contrary to classical evolutionary theory, the processes that drive the small changes observed as species diverge. That's what you might see in natural populations of the software, for instance. Cannot be taken as models for the evolution of body kinds of animals. These are as apples and oranges. There's a fundamental quality of difference between the kind of variation that we see in living things today and the kind of variations that wouldn't be quieter in the Cambrian explosion, let's say, to build those animals in the first place. Now, the global solution which you can find in his publications over the past 15 years is to need neo-Dharmonian theory and branch out and try something new. And earlier today at the hotel, I was looking at this most recent paper in Robert De Penney, the intelligent, Douglas Hurley, and they're really busting out. They're really branching out to try something new. The problem is, I think, there are solutions even worse from the problem they're trying to solve. So, bottom line, this theory has provided a framework for research, and that research has shown that the theory itself has failed. And the question is, where does the biological community go from here? My own view is that intelligence design provides a way forward, but that's something to talk about in the future. Thank you very much. I'm going to make this very brief because like Paul, I enjoy the Q&A more than any other part of the evening. A fundamental aspect of neo-Dharmonian theory is that DNA mutations can create new organs and body plans because DNA controls embryo development. As Paul pointed out, DNA mutations early in development are likely to be damaging or fatal, but even if they weren't, they would still not be able to create new organs and body plans because, as I hope to show you in the next five minutes, DNA does not contain all of the information required for embryo development. These are pictures of cells, living cells under a microscope. They look so different from each other morphologically or atomically, and they're so different chemically that without knowing better you might say that they come from different species. But actually, all of these are cells from the same human being. And they all have basically the same DNA. Why are they so different from each other? The process that developmental biologists or the name that developmental biologists give to this process is differentiation. All the cells in the body inherit the same DNA from the fertilized egg. But, later in development, cells become very different. So a brain cell is very different from an intestinal cell. Where do those differences come from? They cannot come from the DNA sequences, which are the same in all the cells. Instead, they come from spatial differences in the embryo. These cells in one part become brain cells, and cells in another part become intestinal cells. This need for spatial information has been known for decades. It's a real problem for embryologists. This is an experiment from 1924 when Hans Speymann and Hildemangel transplanted a piece of a frog embryo from this embryo to that embryo. Now, this lip here corresponds to that. So they took this section of the surface of the embryo and gave this embryo a second what they called organizer. And the result was a twin. That is a double embryo, a double axis. The DNA was not changed. And there have been many experiments like this that have been done. I've done some myself. What about I'm making this very fast, what about those of you who have studied biology may have heard of these. Mutations in Hox genes can have dramatic effects on anatomy. For example, mutations in one of them can transform the balancers behind the wings of a normal-proof fly into normal-looking wings. They look like they're not functioning because they have no muscles. So this fly is actually severely disabled. But it's a very impressive change. Here, mutations in a different gene can change the normal antennae which in these little red spots, the eyes are up here, can change these antennae into legs. Again, the fly has a hopeless cripple. But the effect of the mutations is very dramatic. But they're not changes in body planning. As Paul pointed out, arthropods, these are just two of the many phylobit appeared in the Cambrian, and arthropods have an external skeleton, the blue, and a ventral or abdominal nerve cord. Cordates, like us, have a soft body with an internal skeleton and a dorsal or back nerve cord. This is what we mean when we talk about differences in body plans, not whether you have antennae or legs coming out of your head. Paul also pointed out that there's a hierarchy of genetic effects here. Hox genes actually kick in long after the body plan is formed, long after we already have approved life. But I'm going to argue in the next two minutes that even these earliest genes act within an already established body plan. For example, those first two genes in the list in the previous slide were Bitcoin and Nanos. These genes determine the location of the head and the tail in the proved fly embryo. This is the egg, by the way. These are the nerve cells that give rise to the egg.