"Best" evidence for evolution.

There is a clear example of evolution by mutation in one of the very next examples you posted - dog breeds. Several annoying yappy little breeds of dog have bizarre little stumpy legs, and researchers have identified the gene responsible for this condition. It's caused by a duplication of the FGF4 gene on chromosone 18. The important thing here, is that this is a dominant allele. A dog which inherits the FGF4 retrogene from either parent will have stupid little daschund legs, regardless of what it inherits from the other parent.This is not a trait we have created in dogs by a novel shuffling of alleles. It's a trait not present in wild wolves, and since the allele is dominant the allele cannot be present in wild wolves either. It's presence in modern domesticated dogs means either that there were, once upon a time, a wild population of stumpy-legged little canines that interbred with domestic dogs but left no trace or, much more reasonably, that this duplication emerged by mutation somewhere along the domestic dog lineage.

The reason this was the trait I thought worthy of mention was the fact that it was so unlikely to be adaptive in a wild population. That, coupled with its dominance, is the reason it's easy to establish that it is, in fact, a novel genetic change which arose in a domesticated population.By the way,

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the beneficial results one would assume would dominate if mutations really were the source of evolution

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is not, in fact, what we would assume. The more beneficial a mutation is, the faster we would expect it to be driven to fixation. This means that an allele with clear, obvious and uncontroversial selective benefiit would be one of those least likely to show any variation in an existing population - meaning its one not suited to a quick example of adaptive mutation.But this is all irrelevant. Once you've accepted the existence of deleterious mutations, you've accepted the possibility of adaptive mutations. If changing an A to a C is deleterious, then a mutation which changed a C back to an A in the suceeding generation would be advantageous. Problem solved.

Faith seems to be under the impression that there is a gene called 'eye colour', and so if it mutates the only phenotypic effect it can have is to produce a different eye colour.

The point is not only that multiple genes are involved in eye colour, but that there is no gene that's involved only in eye colour.Genes make proteins. Some of these proteins are the substances out of which our bodies are made - collagens, actins, myosins, keratins etc. Other proteins are not structural ones, but are involved in the biochemistry going on within and between cells. This category would include transcription factors, like the Hox genes you mentioned earlier. Transcription factors are involved in transcribed DNA into RNA - a step in the process of turning a gene into a protein, and so are very important in development. Different activity of transcription factors plays a big role in deciding what genes get expressed where, and so explaining why you have different types of cells forming different structures when they all have the same DNA.Why does any of this matter? Because very similar genes make these proteins in different species (and a different places in the same species). The structural stuff we're made out of is not so different. Myosin II in the skeletal muscles of a rat is pretty much the same as in a human; as is the myosin II in the heart of both species. And they're both made by very similar genes.And the same goes not only for the structural proteins, but for things like transcription factors that help to decide how these structural proteins end up being distributed around the developing body - how the heart ends up being a particular shape. Transcription factors with the same binding domains can be involved in all sorts of different developmental processes, both within the same species and across different species.Mutations in Hox genes do not just swap legs for antennae - these are just dramatic obvious mutations which first helped to identify them (they are where the word 'hox' comes from - it's shortened from 'homeobox' where the 'homeo' refers to homeotic mutations - ie. a mutation which causes a part to develop as a diffferent part). Nor are hox genes the only transcription factors (not transcription factors the only types of gene involved in DNA regulation). Changes in these genes can cause all sorts of changes in development.In summary - the same structural genes, and the same regulatory genes, with some changes in sequence, produce very different animals. How, then, do we not have a mechanism for changing one species into another?

Well, the same basic chemistry makes a human hand and a human foot. Why don't they look the same? Because regulatory genes adjust the expression of genes at different places and times in development. We know that another family of transcription factors are involved in this - the T-box genes. Tbx4 is mostly expressed in the leg and Tbx5 in the arm.Arms and legs are, of course, made of the same proteins, and also the same structures - the basic pattern of bones in the arms and leg is clearly the same; they just develop different relative sizes and shapes. And that's because of the genetic pathways (of which the T-box genes are an important part) causing different genes to be expressed more or less at different times of development. That causes bone to be laid down at different speeds at different places and thus they form different shapes.And that's not much difference here with chimp feet and human feet. They also have the same pattern of bones, just these are of different sizes and shapes - just as they are between the human hand and foot, and between the chimp hand a foot. Slight changes in the behaviour of transcription factors and signalling molecules will cause changes in the expression of genes at different times during development, causing different bones to grow at different rates and thus assume different shapes - making a chimp's foot look different to a human foot.But this is where conversation with you gets weird. Because you don't find this process mysterious at all. You think it's perfectly normal for the same structures to grow at different rates and into quite different shapes, as long as it happens on trilobites. I can't understand why you think this change in the size and shape of bones is impossible: while the obviously much greater difference in size of shape (and, for that matter, presence and absence) of carapace elements here is not at all problematic:

We could give you an exact list of mutations that would turn a chimp into a human, because we have both genomes in full. But that wouldn't be instructive. It would also be overkill, since it would include much that was unnecessary, and wouldn't actually tell you which changes were necessary to get a human looking foot.But I'm baffled why you expect me to be able to give you the specific mutations necessary. Do you know the genetic developmental pathway that causes the chimp genome to produce a chimp foot? Me neither. This does not reflect badly on us - the details of this are not understood by professional geneticists either. Development is extremely complicated, and there are people who've spent careers unraveling the genetics behind the development of the vulva of a tiny little roundworm - a microscopic organ that consists of about 20 cells.If we don't understand how the pathway currently works, how can we describe how it could change?If you're just looking for hypothetical ideas of the type of mutations, then of course we can speculate. Since the feet of chimpanzees and humans are so similar and consist of all the same parts, all that you need to move the relative positions of the parts is for bits to change the rate and/or timing at which certain bits grow during development. We even have some clues where to look here, since we do know the genes which set the patterning which makes toes develop in different ways - shh and certain Hoxa and Hoxd genes. But you probably don't want to change these, as they're fundamental to all sorts, but the some of the genes which they transcribe are clearly setting in place processes that cause different toes to develop in different ways.So those genes, or the ones they in turn transcribe, or inhibit, are the ones you'd need to change. A point mutation which reduced the activity of a specific gene, for example, would mean that it produced less of it's protein - if that protein is what's causing bone to develop at a particular speed in a particular location, then this would mean that would happen slower, and you'd end up with a differently shaped foot.Or you could have the same effect not by changing the activity of the gene itself, but by recruiting another gene into the process which inhibits how that gene work. Development is full of genes that inhibit the activity of others and this is one of the reasons developmental genetics is so complex. You can change a process one way by inhibiting a gene, then change it a different way by inhibiting the inhibitor, then change it back by inhibiting the inhibitor of the inhibitor. And so on. Yes they are. Of course they are. I'm not sure how to respond to such an odd statement except with 'look' (note to avoid confusion that that's a right chimp foot and a left human foot):

So, to review, these are all the same, just different shapes. And these, too, are all the same, just different shapes. But these are completely different and totally unrelated because they're different shapes. Hard to take you seriously if you're claiming that with a straight face.

I'm not trying to catch you out in some kind of wordplay and sophistry. This isn't a trick. Those trilobite pygidia are more different from one another than the bones of chimp and a human foot are. This is just obvious.But whether we agree on the degree of difference is not important. The important thing is that we have all the same bits. For a mutation to change the shape of bits it just needs to make a change in the speed, or the start or end, of a molecular process during development. The same as what causes dogs to have such a weird variety of shapes. OK, now I think I understand the objection you were trying to make. You're simply arguing that no intermediate form could be viable - you have to have the whole package at once.But that's not true. I unfortunately don't have a good hypothesis for you, since I don't have a good explanation for human bipedality, but the bits do not have to all come at once. You could walk upright with a chimp's foot. It wouldn't be as efficiently as we do, but that very fact is what would create the selective pressures to change the foot once the shift to regular bipedalism has already happened - most of the changes in the foot would probably follow the changes in the pelvis.I think it's common to underestimate the behavioural flexibility of many animals. Animals can, and do, do all sorts of things they are not particularly well designed for. If this allows them to exploit an unexploited niche, then they can succeed at it despite not being very good at it. Being in a situation where there's a mismatch between anatomy and behaviour creates a selective pressure for change in anatomy - things that could have been deleterious previously could not be beneficial. And once one thing changes, it then puts pressure on other things to change so as to work better with the changed bit. Which might then put pressure on other bits to change, or which might allow the original change to be pushed further.

Changing the shape of the bones changes the shape of the rest of the tissue as well. The development of these things are not separate - you don't need one mutation to change the orientation of a thumb bone and a separate one to change the orientation of the overlying skin - the same changes to signalling molecules will affect the development of all the bits of the limb.If you mean that the structure of flesh is different, then you're right, but in what way? The myosin fibres that make up chimpanzee muscle are almost identical to those that make up human muscle. The main difference between human and chimp muscle stem from the fact that proportions of different types of myosin. There are three main myosin molecules that make up both human and chimp muscles. Chimp muscles contain a pretty even amount of all three, while one of the three, MHC I, makes up more than half of human muscles.The genetic basis of this difference is apparently not known, but doesn't need to be anything too complicated. These different fibres are produced by different (but related) genes, and like I already mentioned, there are lots of ways to change genes, or their promoters or inhibitors, to make them produce more or less of their product - the products in this case being muscle fibres.The differences in tissue between humans and chimps are just as much a matter of shuffling of parts as are the differences in the position of bones. There's a lot more difference than 'clumping of spines'. Half of them don't even have any spines, and yet are noticeably very different from one another. You've mentioned your having problems with vision - can I recommend zooming in to see them properly?I would be extremely surprised if they were all constructed from identical tissue, but that's probably very difficult to tell from fossils. But I'm more interested in how you can tell these can all be produced by 'the same genome'. What's your criteria for figuring this out? Dog skulls all came from dog genomes yes, because they're all dogs. But 'the dog genome; is an abstract concept - there isn't really any such thing. Every dog has a DNA sequence unique to itself.And we know that sequence can change - by mutation. This isn't speculation - it's fact. Dogs have probably had their genes sequenced more than any animal other than humans and the classic laboratory subjects for genetics like D. melanogaster and C. elegans; so we can see that dogs have some sequences in their DNA that were not inherited from their parents - mutations change DNA sequence - indisputable fact.And we know that changes in DNA sequence can have phenotypic effects. We've identified many in dogs. The weirdly shaped face of a modern bull terrier is likely due to a unique tandem repeat sequence in the Runx-2 gene, this doesn't exist in other breeds, and it doesn't exist in the DNA of a bull terrier which died in 1931 (and we know from old pictures that bull terriers then did not possess the same weird facial shape). It seems likely this is a mutation that arose in this breed in the 20th century; and it causes phenotypic change.If DNA sequence can change by mutation (which is an undeniable fact) and if changes in DNA sequence can cause morphological change (which is an undeniable fact) then mutations are causing morphological change. The shape of the bull terrier's face was not already hanging around in the genome if the specific sequence that caused it did not previously exist.

Then see above. The process of changing the shape and orientation of the bones will also change the shape and orientation of the flesh - it's not a separate matter. I feel like I'm missing the point you're trying to make, but have no idea what it could be. Yes, you do - humans and chimps. What does one have that the other does not? Well, I would agree that what makes a goat a goat and a horse a horse is what makes them separate species. I'd have several species of goats, but that's not the point here.They still have the same basic parts. That's how I would describe the differences between horses and goats, by listing the ways in which those same parts differ. I mean, there are some things goats have that horses don't - horns are an obvious one - but that's not really the key difference. Not all goats have horns, but that doesn't make them look like horses.Some things one of the other has more or less of - goats have more vertebrae, and more digits. They have canine teeth, but so do some horses. Horses have upper incisors, which goats don't.Most things are present in both, but sometimes differ in shape. Goats have more complicated digestive tracts; horses have three trochanters on the femur, goats only two. Horses have a channel running through their alisphenoid bone; it's fused shut in goats.But it's all the same basic parts. That's what enables us to talk about things like an 'alisphenoid' bone. I couldn't talk about the alisphenoid of a trilobite, but goats and horses clearly both have them.

Horses and goats are, of course, much more dissimilar from one another than humans and chimps are. I'm struggling to decide if there's any point in going into detail on this. Of course a chimp with human skin would not look like a human! Because it would have chimp bones and chimp muscles. Bones and muscles which are clearly the same parts in humans and chimps, just slightly different shape and slightly different composition. I would disagree - the flesh doesn't that look different at all. I think what you're referring to is simply the fact that the metatarsals are obscured by skin and muscle, which makes the difference in orientation seem more dramatic and obscures how similar the digits are to one another. And since you said something about soles, earlier - you're probably also focusing on the crease lines (not sure if there's a proper word for that) in the chimp foot. But these are simply a result of the shape and orientation of the foot - the fact that it's shaped to grasp like a hand. It's not something extra, separate from the shape of the bones - it's simply a consequence of their shape.

Possibly because differences that are not explicable in terms of anatomy, nor visible in pictures, don't actually exist. They're just something invented in a desperate attempt to maintain an special creation for humans.

There are no human genes that differ from the equivalent gene in the chimp by thousands of changes. Human genes differ from their mouse equivalents by a little more than a thousand changes on average.I don't understand why you think just randomly guessing at numbers is the way to figure these things out. Why not investigate the findings of all the people who've spent careers getting the real answers by actually looking at real genomes and seeing how they work? It's all really quite fascinating (although very confusing), and more educational than pulling ideas out of thin air.

What Faith's trying to describe is the idea that has been mooted in regards to, for example, the dog breeds formally recognised by Nazi-dog societies like the American Kennel Club. These things have only existed for less than two centuries, hence the idea that the phenotypic variation between the breeds can be explained solely by a partitioning of the standing genetic variation of 19th century domestic dogs.It's not an inherently ridiculous idea, even though it is in fact wrong even in this specific instance of extremely recent, extremely fast directional selection. There are strong candidates for de novo 20th century mutations within dog breeds, causing noticeable morphological change, that have been subseqently selected for. I mentioned earlier the mutation in the [i]Runx2[/] gene in English bulldogs.Trying to account for all variation in a Faith-species this way is ludicrous, of course.

This presumably being an ecology which evolves via the dialectical method.