The Truth of Evolution

[axeplayer]

Hello everyone. I'm not sure if this has been brought up before in the forum, so if it has, forgive me. But I was wondering if any of the evolutionists out there could answer this question for me......do you know of any truths that exist in the theory of evolution? In other words, is it purely based on speculation and the combination of completely different fossils to make it look like gradualism? Or is there actually truth to it?

[Ilurk]

I wrote:

A dung beetle native to France was introduced into both the North America and Australia. That is, dung beetles from one population (in France) were carried thousand of miles from their place of origin and set loose on two separate continents (North America and Australia). The three populations of beetles, all originally from France, diverged. They became different over time. The dung beetles in North America and the dung beetles in Australia, which both started out in France, now look different from each other. And both look different than the dung beetles in France. Do you get the drift? One population yields two populations that are physically different from each other and from the original population. What happened here? What’s it called? I’ll let you fill in the blank. It’s called _______________.

Axeplayer responded:

ok, you obviously didn't see my last post, so i'll explain it again. The dung beetles that look differently from one another are not the original dung beetles that were brought to the continents. They're the offspring of the originals. The French dung beetles mated with the american and australian dung beetles to produce an interbreeded population of dung beetles. If you gathered a group of, say, 200 single caucasian north americans, and shipped them off to japan, and told them "do what you want", wouldn't it be likely that at least half of them would reproduce with a Japanese partner? according to you, that would be evolution. but it is not. and here's where I fill in the blank........What happened with the beetles? What's it called? It's called reproduction.

No Axe, I saw and read the entire post, which is why I responded the way I did. And the post above just continues to demonstrate your profound ignorance of even the most basic knowledge of biology.

Now let me ask you something Axe. Did you read my entire post? Did you read the part where I pointed out that the American and French Dung Beetles were different species, you know, like sparrows and robins, and that your contention that the two species mated and produced viable offspring was, to be kind, questionable. Here is the section of the post you seemed to miss:

Now, if you think that it’s not evolution in the case of the dung beetles or speciation in the case of the house finches – as you seem to be claiming – I suggest you point us to some real evidence that supports your contention. Merely claiming something might have happened - that the native American beetles (not African, right) mated with the French beetles – and produced another kind of beetle doesn’t exactly cut it. Raises a bunch of questions, you know, like considering the American beetle and the French beetle were separate species, how could they have mated and produced viable offspring? Little things like that. And then there’s the problem of actually getting the genetic evidence to support the claim…

Whoa! I just read your last post, Axeplayer, and truly, you know absolutely nothing about biology. What you said was stunningly incoherent. But I’ll give you a chance to redeem yourself. Please, direct us to the study you did on North American and French dung beetles that confirms the two species mated and produced viable offspring, and that the divergence of the French dung beetles in North America was a result of the hybridization of the two species.

Read it? Good. Now how about responding to my direct request for data supporting your contention that the two separate species of North American and French Dung Beetles mated and produced viable offspring, and that the divergence of the French dung beetles in North America was a result of the hybridization of the two species. And while your at it, how about evidence that any species of North American Dung Beetle can mate with any species of Japanese Dung Beetle and produce viable off spring.

Don't make anything up. Don't guess. Find and post real evidence. You know where the ball is.

[micatala]

"Formed by artificial selection." Nothing artificially "created" proves soemthing happened by random chance. That's one minus one equals plus seven. Why" Because I placed nine things BEFORE I took away two.

Doesn't "formed by artificial selection" mean, designed? It certainly means artificially selected. No?

More than one genus of insects? There not still and only insects? Are any of them changing into mice or some other kind of similar sized other-than-an-insect creature?

Isn't timeframe problems an excuse? Especially since the lab can
"artificially" reproduce and create?

Just a technical note, AlAyeti. If you use the QUOTE button when copying in portions of others posts, your posts will be a little less confusing. Simply click on the QUOTE button, then copy in the text after, then click the QUOTE* button to close. You could add in

to identify the person quoted.

I would agree that having species produced by artificial selection does not prove the same species (or any species) has arisen by natural selection. However, artificial selection, since the genetic basis is THE SAME as in natural selection is not irrelevant, and in fact provides substantial plausibility, all by itself, for natural selection. The only difference is that humans are manipulating the selection process instead of selection occurring due to natural or environmental factors.

Artificially selected is not, in my mind, the same as 'design.' When something is referred to as design, I think of it as having its pattern made 'from scratch.' This is not really what happens in artificial selection. In the latter case, we usually amplify certain characteristics of the existing species (longer legs, shorter nose, thicker fur, etc.)

The time frame problem is not an excuse, it is simply reality. Based on fossil evidence, radiometric and other dating techniques, etc., we have a reasonably good idea of how long it takes for species to undergo major morphological changes. The fact that these time frames are so long as to be unobservable in 'real time' in no way negates the existing evidence or weakens the argument. It is just the nature of how things work.

It seems we have shown that species can evolve into other species in fairly short time frames, and now you are changing the subject and asking us to show genus or higher order change. I don't think anyone has claimed that the larger changes you might be looking for (eg. reptile into mammal) can or have taken place on short time scales. This doesn't mean that they cannot or have not occurred. The fossil evidence overwhelming indicates that they have.

[Gollum]

Doesn't "formed by artificial selection" mean, designed? It certainly means artificially selected. No?

Well no it doesn't. If I took you into an automobile show room and invited you to select the car you wanted and you picked the BMW, that doesn't mean that you designed the BMW. You would probably have only the vaguest of notions about how it was designed or how it worked. Your selection criteria (Man! Would I ever look cool in that!) have nothing to do with the automotive designer's criteria about how to design or build it.

Similarly, nature's selection criteria (Does it enhance the capacity to reproduce?) have nothing to do with the mutation mechanism (knock this genetic sequence out and replace it with that one.)

More than one genus of insects? There not still and only insects? Are any of them changing into mice or some other kind of similar sized other-than-an-insect creature?

Of course not ... just as the gravel truck doesn't change into a formula 1 racer ... but all vehicles that we see today are probably based on something like the Ford Model T. Four wheels, an engine, steering wheel, a cab with seats, etc. Evolution is the theory of common descent ... we come from common ancestors. Our contemporaries are not ancestors.

Especially since the lab can "artificially" reproduce and create?

Hadn't heard that one. As far as I know, no lab has ever been to create life nor to do much more than witness reproduction as opposed to making it happen without living organisms as the starting point.

[Jose]

ok, you obviously didn't see my last post, so i'll explain it again. The dung beetles that look differently from one another are not the original dung beetles that were brought to the continents. They're the offspring of the originals. The French dung beetles mated with the american and australian dung beetles to produce an interbreeded population of dung beetles. If you gathered a group of, say, 200 single caucasian north americans, and shipped them off to japan, and told them "do what you want", wouldn't it be likely that at least half of them would reproduce with a Japanese partner? according to you, that would be evolution. but it is not. and here's where I fill in the blank........What happened with the beetles? What's it called? It's called reproduction.

Ah, I see. I won't complain about not reading my previous post, because sometimes even I can't stand to read what I've written. The bottom line is: different species cannot interbreed. The current beetles are the offspring (ie descendents) of the French beetles, as you say. But they could not mate with the American and Australian beetles. They reproduced according to their kind--and through mutations, changed as they did so.

The native beetles have been isolated from the ancestor of French/American/Australian dung beetles for millions of years. They are different species. Humans, on the other hand, are so recently evolved that we haven't had time to speciate. Had we failed to invent seafaring ships or airplanes, maybe we would become different species sometime. So far, however, we have not. Nor are we likely to, now that there is so much interbreeding.

So, your example fails: you are using variants of one species to explain the behavior of different species. This is understandable if you don't know the biology and evolutionary history of dung beetles.

Question. If the same kind of beetle or bird has a number of individuals that seperate from the collective or group and form mating habits and behaviors different from the original condition, how does that qualify as evolution?
Are they a different kind of lifeform?

Well, this qualifies as evolution because of the definition of evolution. There has been genetic change. It occurred over time. Therefore, it's evolution. What you are confusing with "basic" evolution is the consequences of evolution carried out over millions of years. You may also be confusing evolution with the misconception that evolution should mean animals going *pop* and becoming some other kind of animal that now exists. It doesn’t work that way. The bottom line is: any genetic change in a population that occurs over any length of time is evolution. The creationists call this microevolution, and accept it as truth. It's the only way they can explain Noah's 8000 species becoming todays' millions of species.

To be fair I think a lot of distinctions were made early in this discussion to confuse the matter here. Evolution is Change over time. But the mechanism should be nailed down. For instance, the mechanism of polyploidy in various plants was put forth as a justification for speciation. This is change over time, however it is highly accelerated and does not have a corresponding mechanism outside of the plant kingdom. If the mechanism being proposed in the animal kingdom is mutation and selection then we should be relegated to basic genetic systems when talking about types. Certainly, species could arise by choices in practical breeding, which is what I think I am hearing in your example Jose. But for a real "species" in my mind to arise, the gametes would only match up with matching gametes of the same type. The cells in isolation would no longer pair with the previous beetle and would pair and make viable offspring with its own type. ...

As it turns out, there are many mechanisms. Plants happen to be able, on rare occasions, to become polyploid, or for one species' gamete to fuse with a closely-related species' gamete, and create a hybrid that is a new species. This is how we got wheat (look up its history in McGee's On Food and Cooking, which everyone should have).

Animals generally don't do that. There are many other barriers to inter-species mating, from behavioral (courtship displays and songs in birds, for example) to the jelly coat around the egg, which the sperm must penetrate (which can sometimes be removed in the lab, to produce inter-species hybrids). All of these count as genetic mechanisms of speciation, and as part of evolution.

There is also the question of how big a role natural selection plays. Sometimes, it's great. Other times, it's not. There's a lot of genetic drift as well--genetic variations that get "fixed" in the population due to random chance. You know, in an isolated small population, if one male gets killed, and the other 5 have offspring, you lose all of the genetic variation in that one who got killed. There is also close linkage--in which a favorable gene is very close on a chromosome to a gene that is responsible for some irrelevant characteristic (like tongue-curling, for which I can't think of any value at all). Selection for the "good" gene co-selects for the irrelevant one.

To make the mechanism absolutely clear, here are the rules:

1. traits must be heritable. This means: dependent on DNA.
2. mutations must occur, to give genetic variation of traits. This cannot be prevented, and is a given for every genetic trait. (For polyploidization and hybridization in plants, there must also be mistakes in normal mechanisms--cell division, for polyploidy, or breakdown of the normal species restriction for hybridization. These nonetheless result in genetic variation.)
3. some individuals have more offspring than others.

That's it. If these conditions are met, evolution must occur. There is no way to prevent it. Call it microevolution if you like. Whatever you call it, it cannot be prevented for anything that depends on DNA.

The above quote from AlAyeti suggests that "evolution" must cause creatures to become wildly different. There is no such requirement. This is a fable invented by the anti-evolution crowd. Why? Because acceptance of the basic rules, combined with thinking, leads to the inescapable conclusion that evolution happens, and that common ancestry must be true. We can quibble with the extent of common ancestry, perhaps, but some level of common ancestry must be accepted. Those three simple rules above guarantee it.

For common ancestry, we pretty much have to go with DNA similarity. The species with the most similar DNA must have the most recent common ancestor. OK. Wheat, rye, and barley have a common ancestor. No problem. Peppers, tomatoes, and potatoes have a common ancestor. Still no problem. Wheat, rye, barley and corn? That's a bit more difficult, since corn originated in the Americas and the others in Europe. Still, DNA similarities tell us there must be a common ancestor. They are all grasses. Peppers, tomatoes, potatoes, and eggplants? Same logic: the first three originated in the Americas, the latter in Asia, but the plants all look pretty similar, and the flowers do, too. They're all Solanaceae, with the same neurotoxin in their leaves.

It seems, somehow, to get touchy with animals. Humans and chimps? Their DNA is extremely similar. They must have a common ancestor. Humans, chimps, and mice? Again, there is a lot of similarity. They must have a common ancestor.

If we are to believe the creationist story that Noah's 8000 species became today's millions of species, then common ancestry like this must be true. The only question, it seems, is how far back to push the common ancestor. Creationists like to stop early, with the species Noah had on the ark. However, the logic that gets you back to those "kinds" of animals works equally well if you go back farther.

And so it goes. DNA is the key, because of those 3 simple rules above. From DNA similarities, we find that every living thing on Earth is genetically related. This provides remarkably strong evidence for a common ancestor of all living things, whether or not we are willing to accept it. The funny thing is, if we make a "tree" of relationships based on DNA similarities, it comes out the same as if we make the "tree" based on morphological characteristics. Even more surprising, the branches of the DNA tree, if the tree is superimposed on a geological timeline, kinda match the fossil record. You know--the mammal/reptile branchpoint is moderately far down the tree, and happens to be about where we'd put an age of some 250 million years ago.

And all of this just from those 3 simple rules. What's hard for people to grasp is the mechanism by which genes determine characteristics, the mechanisms by which different characteristics result in having more or fewer offspring, and the logical consequences of this simple biology carried out over a long, long time.

[youngborean]

If we are to believe the creationist story that Noah's 8000 species became today's millions of species, then common ancestry like this must be true. The only question, it seems, is how far back to push the common ancestor. Creationists like to stop early, with the species Noah had on the ark. However, the logic that gets you back to those "kinds" of animals works equally well if you go back farther.

And so it goes. DNA is the key, because of those 3 simple rules above. From DNA similarities, we find that every living thing on Earth is genetically related. This provides remarkably strong evidence for a common ancestor of all living things, whether or not we are willing to accept it. The funny thing is, if we make a "tree" of relationships based on DNA similarities, it comes out the same as if we make the "tree" based on morphological characteristics. Even more surprising, the branches of the DNA tree, if the tree is superimposed on a geological timeline, kinda match the fossil record. You know--the mammal/reptile branchpoint is moderately far down the tree, and happens to be about where we'd put an age of some 250 million years ago.

But the mechanism is not consistent. This is my point. For dealing with animals we do not have the recreatable mechanism to describe large Chromosomal Changes (although many proposed theories exist). And all deficiencies generally result in termination or fertility problems. To make it general and then to assume it operates in a similar fashion in animals is limited. As far as the genetic tree matching the phylogenic tree, aren't there numerous cases of anomolies in every branch (certain lines not showing a direct progression in chromosome number)? Such as wild chromosome numbers etc. To say that repeating patterns inherently says common ancestor is a stretch to me without a recognizable mechanism to advance the evolution of animal genetic matter, I personally would argue that the factor for genetic speciation should be whether 2 gametes chromosomes are able to line up, and not the enviromental product of their genes (egg types, courtship displays) which you suggested. These only show differences in how their genes are expressed, unmatchable changes in genotype vs phenotype. To go back beyond kinds, based on what we know of animal genetics is extremely difficult because Mutation plus natural selection giving rise to traits has very little weight in describing a viable way that chromosomes progressed in the animal kingdom. I.e. we have not seen polyploidy work in the animal kingdom.

[Jose]

But the mechanism is not consistent. This is my point. For dealing with animals we do not have the recreatable mechanism (1) to describe large Chromosomal Changes. And all deficiencies generally result in termination.(2) To make it general and then to assume it operates in a similar fashion in animals is limited. As far as the genetic tree matching the phylogenic tree, aren\'t there numerous cases of anomolies in every branch (3)(certain lines not showing a direct progression in chromosome number(4))? Such as wild chromosome numbers etc. To say that repeating patterns inherently says common ancestor is a stretch to me without a recognizable mechanism to advance the evolution of animal genetic matter, I personally would argue that the factor for genetic speciation should be whether 2 gametes chromosomes are able to line up, and not the enviromental product of their genes (egg types, courtship displays) which you suggested. These only show differences in how their genes are expressed(5). To go back beyond kinds, based on what we know of animal genetics is extremely difficult because Mutation plus natural selection giving rise to traits has very little weight(6) in describing a viable way that chromosomes progressed in the animal kingdom.(7) I.e. we have not seen polyploidy work in the animal kingdom(8).

I'll comment here, based on the numbers I inserted above. I didnt' want to break up the paragraph.

1. A "recreatable" mechanism is not necessary, and probably isn't possible. We can certain induce chromosomal changes with X-rays, and we know that many cancers are the result of chromosomal rearrangements. To ask to recreate a specific rearrangement is asking for a large number of low-probability events to occur again in the same sequence. Nonetheless, we can, and have, recreated the mechanism--X-ray induced rearrangement.

2. True, most deficiencies are lethal. But some are not. Nor are about a third of inversions. Like mutation in general, it isn't legitimate to go from the fact that most are deleterious to the conclusion that all are deleterious.

3. In the past, there were a number of discrepancies between trees built on physical characteristics compared to trees built from DNA or protein sequences. The same could be said for trees built from physical characteristics alone, or from DNA sequences alone. The explanation is that these were based upon a small number of characters--where small means a lot, but fewer than was necessary. With larger data sets, the discrepancies have been resolved.

Several sources of the discrepancies are these: physical characteristics can converge or diverge rapidly, due to minor mutations in gene regulation. Many are subtle and difficult to distinguish unambiguously. Protein sequences provide a clear evolutionary history of that protein, but not necessarily of the organisms that produce it. The same is true of DNA sequences for single genes. This is because gene duplication is common, as is DNA rearrangement that breaks genes and fuses them into gene hybrids.

Also problematic is the fact that some eukaryotic genes descend from the archaea and some from the eubacteria. This is that favorite problem of endosymbiosis. The DNA data tell us clearly that mitochondria descend from a eubacterial cell that became trapped in an archaeal cell. Over time, genes from the trapped bacterial cell moved to the nucleus (we still don't know how). Thus, trees made from genes that derived from the eubacterial ancestor link eukaryotes to the eubacteria, while trees made from genes derived from the archaeal ancestor link eukaryotes to the archaea.

The solution has been to use more genes, to build a larger data set. It has also been done to use both sequence data and morphological data to develop a very large data set. The latter provides trees that are extremely robust (ie, if you remove a species or two and re-calculate the tree, you get the same result).

In short, the discrepancies among trees result from inadequate data, and inefficient algorithms for building the trees. As both have improved, the discrepancies have become far fewer.

4. Chromosome number turns out to be irrelevant. I know that it is taught otherwise, even to the extent that our State Standards insist that we teach that chromosome number is important. The fact is, however, that it is not. X-ray induced gene rearrangements can, and have produced chromosome fusions with no loss of information. All we're talking about here is telomeres on the ends of the DNA, to assure replication of the ends of the molecule, and centromeres to assure microtubule attachment at mitosis. It's no big deal to break one chromsome just inside from the telomere, and another right next to the centromere, then move the entire arm of the second chromosome onto the end of the first chromosome. This kind of thing happens. As a result, mammals, which all have pretty much the same genes, can differ dramatically in chromosome number.

But the number of chromosomes says nothing about the genes that determine the plant or animal's development. Thus, chromosome number says nothing about genetic relationships.

Certainly, the first mating of an animal with a chromosome fusion to animals with normal chromosomes will produce an aneuploid zygote that will probably die. So, there must be a way that these chromosome fusions (or chromosome break-ups, for that matter) have been passed on. I don't know what this might be. When I was working with Drosophila, I occasionally found fertile offspring from matings of chromosome-fusion and normal parents, presumably from a chromosome-fusion gamete fusing with a gamete in which meiosis had not gone correctly. This indicates that it is possible. I presume something like this has occurred in the wild.

5. Chromosome alignment at meiosis depends on DNA sequence identity, and not on whether the DNA is stuck to the same centromeres. Rearranged chromosomes can pair and align quite happily--it's just that they don't do so like two sticks side-by-side. They bend and fold to allow identical sequences to find each other.

What really matters is not the chromosomes, but the genes themselves. As long as there is a way to get equal complements of the genes from both parents into the progeny, then you're fine. But, the genes must be the same, and must be reulated the same way, or you get problems with embryonic development. That is, the way the genes are expressed is critical.

When we speak of animals being different species, we refer to their inability to produce fertile offspring. If they are very different, like squirrels and wildebeests, this seems obvious. When they are very similar, like meadowlarks or house finches from the eastern and western populations, we can quibble about it. Maybe their gametes could fuse and produce fertile offspring if they ever had the chance, but if the populations have different courtship rituals or songs, or if they become fertile at different times of the year, then they won't mate, and there will be no offspring. It is often something this minor that provides the initial reproductive isolation between two populations of a species; once they are isolated, and fail to mate with each other, then they cannot share genetic variation, and they will become more and more different.

6,7. It looks like I can't discuss these points separately. If, as I noted above, chromosomes are not the issue, but the genes on them are, then we have no reason to expect any kind of progression of chromosomes through history. Therefore, while you are right that minor changes in individual genes and selection upon those variants has little to do with chromosome number, that turns out not to be a problem, since chromosome number isn't particularly relevant.

On a larger scale, though, chromosome rearrangements are mutations. A mutation is any change in the DNA. In this sense, these types of mutations do impinge fully on the evolution of chromosome number, size, and gene-order. These types of mutations, like any others, are subject to selection--but, like any other mutation, only if they have an effect on the characteristics of the organism.

Chromosome rearrangements like inversions, translocations, or chromosome fusions have effects primarily through the genes at the "breakpoints" of the rearrangements. For example, if we have chromosome ABCDE and chromosome LMNOP, we could get a translocation that gives ABCOP and LMNDE. If moving C next to O affects the patterns of expression of these genes (a common occurrence), then there is something for selection to act upon. It is also common for something like breaking in the middle of gene C and in the middle of gene O, producing a C-O hybrid gene. Very often, these kinds of hybrid genes produce hybrid proteins that exhibit new activities. This is one of the ways that "new information" is produced (even though it doesn't produce new DNA!).

Because many eukaryotic genes exist in chromosomes in pieces that are separated by intervening DNA (called introns), chromosomal rearrangements that break within introns can easily produce hybrid proteins. A great deal of eukaryotic evolution seems to have involved the shuffling of gene bits by this kind of mechanism. This mechanism is also one of the reasons that DNA sequence trees based on single genes can be confusing--a gene we have now may have two ancestral genes, each of which contributed a portion of the current gene.

8. We typically do not see tetraploid animals resulting from hybridization like that of plants. However, triploid and tetraploid animals are known--and have larger cells than diploids, but are not very much larger animals than the diploids. The size-regulation systems depend on diffusion of molecules, rather than on counting cells. I suspect that the difference between plants and animals in this respect results from the fact that animal embryogenesis involves cell movements, which can be easily perturbed by slight genetic changes. Plant cells cannot move, so the controls over development are more restricted. It may be easier to accommodate the mismatches of gene regulation in plants when hybrids form. In any event, you're right that polyploidy is not a common mechanism of speciation in animals.

I consider polyploidy and hybridization between near relatives in plants to be novel speciation mechanisms that are great fun to analyze, but that are somewhat distinct from the basic mechanisms of evolution that affect all organisms. The fact remains that DNA is the genetic material, and that DNA is subject to mutation--base changes, insertions, deletions, rearrangements, etc. Mutations can affect the characteristics of the organism, and can therefore be selected for or against. Gene expression and the regulation of gene expression are the critical in-betweens that connect DNA sequence to selectable characteristics.

It is also essential, for speciation, to have reproductive isolation. This can be achieved physically by separating populations of a species. It can also be achieved behaviorally--but therefore dependent on mutation/diversity--such as changes in mating rituals, or acquisition of a new food source by one genetic variant, or any such thing that allows one subpopulation not to notice another. Once any genetically-controlled mechanism develops to make two subpopulations to stop mating with each other, we have incipient species, which will develop more differences, resulting eventually in outright speciation.

Once speciation has occurred, they can't go back--and can only become more different.

[youngborean]

4. Chromosome number turns out to be irrelevant. I know that it is taught otherwise, even to the extent that our State Standards insist that we teach that chromosome number is important. The fact is, however, that it is not. X-ray induced gene rearrangements can, and have produced chromosome fusions with no loss of information. All we're talking about here is telomeres on the ends of the DNA, to assure replication of the ends of the molecule, and centromeres to assure microtubule attachment at mitosis. It's no big deal to break one chromsome just inside from the telomere, and another right next to the centromere, then move the entire arm of the second chromosome onto the end of the first chromosome. This kind of thing happens. As a result, mammals, which all have pretty much the same genes, can differ dramatically in chromosome number.

But the number of chromosomes says nothing about the genes that determine the plant or animal's development. Thus, chromosome number says nothing about genetic relationships.

So it is you assertion that Chromosomes don't matter, then if all mammals have essentially the same genes as you assert. Shouldn't their gametes be able to fuse and line up according to genotype in vitro? This would seem like a simple enough experiment. I realize that the reason chromosomes line up is due to their like parts, or this seems to be the gist of your argument. But how do genes get to teh point where they no longer would match in vitro. I see your point, but there seems to be a huge hole. Where a genotype becomes unable to match. This would essentially be the gist of what I would call "True Speciation". Now this definition may be unacceptable, but since most gametes of seperate "types" would not match if induced into a cell spontaneously, there must be something causing this blockage.

Chromosome rearrangements like inversions, translocations, or chromosome fusions have effects primarily through the genes at the "breakpoints" of the rearrangements. For example, if we have chromosome ABCDE and chromosome LMNOP, we could get a translocation that gives ABCOP and LMNDE. If moving C next to O affects the patterns of expression of these genes (a common occurrence), then there is something for selection to act upon. It is also common for something like breaking in the middle of gene C and in the middle of gene O, producing a C-O hybrid gene. Very often, these kinds of hybrid genes produce hybrid proteins that exhibit new activities. This is one of the ways that "new information" is produced (even though it doesn't produce new DNA!).

Because many eukaryotic genes exist in chromosomes in pieces that are separated by intervening DNA (called introns), chromosomal rearrangements that break within introns can easily produce hybrid proteins. A great deal of eukaryotic evolution seems to have involved the shuffling of gene bits by this kind of mechanism. This mechanism is also one of the reasons that DNA sequence trees based on single genes can be confusing--a gene we have now may have two ancestral genes, each of which contributed a portion of the current gene.

Right. I am also following this I think. But these rearranged Chromosomes, using the methods you propose. Are they enough to cause the genetic material to no longer match? These rearrangements were amazing to me to learn about, but are they speciation based on phenotype. Because if I remember these change phenotype but the don't usually effect reproduction at the cellular level.

[Jose]

So it is your assertion that Chromosomes don't matter, then if all mammals have essentially the same genes as you assert. Shouldn't their gametes be able to fuse and line up according to genotype in vitro? This would seem like a simple enough experiment. I realize that the reason chromosomes line up is due to their like parts, or this seems to be the gist of your argument. But how do genes get to teh point where they no longer would match in vitro. I see your point, but there seems to be a huge hole. Where a genotype becomes unable to match. This would essentially be the gist of what I would call "True Speciation". Now this definition may be unacceptable, but since most gametes of seperate "types" would not match if induced into a cell spontaneously, there must be something causing this blockage.

There is always more to it, isn't there? For two DNA molecules to align at meiosis, they must have sufficient sequence identity for the "alignment proteins" to put the appropriate parts together. As I understand it, this requires fairly long stretches of DNA, not just single genes. So, the sequences of the genes themselves matter, and also the sequences of the DNA between the genes matter. So do the sequences of "introns," which are transcribed into RNA, but spliced out as the initial transcript is converted to mature mRNA. The "spacer" sequences and the introns have little function besides "being there." Consequently, mutations that change their sequences have no effect on the characteristics of the organism, unless they occur in short, "informative" bits (like the start/stop sequences of genes, or the "splice sites" of introns). So, while mutations that change gene sequences can cause changes in the organism, and be selected against, changes in these regions are passed on. Therefore, when we compare DNA sequences of closely-related species, we find that the genes are pretty much the same, but the introns and spacer regions are quite different.

Therefore, even if the two species can mate and produce offspring (as with horses and donkeys), it is often the case that the chromosomes cannot align properly during meiosis, so functional gametes cannot be produced by the hybrid (mule, in this case).

Different variations of these sequences must arise fairly often within a species, but as long as they occur within a single, interbreeding population, the differences are "swapped" among individuals, and things stay pretty much the same. When two populations become separated for a long time, then the two populations cannot swap DNA sequences, and the two populations may end up with fairly different spacer sequences and introns, even if the genes are essentially the same.

To make a mammal requires pretty much the same genes, albeit with slight differences in some of them. The rest of the DNA can be quite different. This is why we can say that we share more than 90% of our genes with mice, but have much less (80%?) DNA sequence similarity. The genes (and control sequences) are what matter; the rest is variable.

Even within genes, sequences can change without changing the protein. The sequences CCC, CCG, CCA, and CCT all code for the amino acid glycine. AAA and AAG both code for glutamate. With changes like this in the "third position" of a "codon," we can have DNA sequences that are too different to align at meiosis, yet produce the identical protein.

Because many eukaryotic genes exist in chromosomes in pieces that are separated by intervening DNA (called introns), chromosomal rearrangements that break within introns can easily produce hybrid proteins. A great deal of eukaryotic evolution seems to have involved the shuffling of gene bits by this kind of mechanism. This mechanism is also one of the reasons that DNA sequence trees based on single genes can be confusing--a gene we have now may have two ancestral genes, each of which contributed a portion of the current gene.

Right. I am also following this I think. But these rearranged Chromosomes, using the methods you propose. Are they enough to cause the genetic material to no longer match? Are these hybrid protiens enough to cause only new like parts to match. These rearrangements were amazing to me to learn about, but are they speciation based on phenotype. Because if I remember these change phenotype but the don\'t usually effect reproduction at the cell level.

The hybrid proteins don't affect the alignment of chromosomal DNA at meiosis. That is determined entirely by the DNA sequences that are involved. The hybrid proteins themselves affect the cells in which they are produced, sometimes making those cells behave quite differently than before. These kinds of DNA changes (mutations, really) are responsible for some of the morphological and biochemical "inventions" that have occurred in evolutionary history.

Bear in mind that most of these kinds of rearrangements produce whacky proteins that don't work, and can also destroy the original proteins. Thus, like most other mutations, they are usually deleterious. However, some can be beneficial. I'd have to look around pretty hard to find examples, but I know that the folks who study this stuff have found a great many.

So, there are several types of things going on here. There is the gradual change of DNA sequences, in essentially a time-dependent manner. For sequences whose function is to be "spacers," mutations probably accumulate in a fairly linear fashion because there is no selection against DNA sequence change.

In genes themselves, changes occur at the same rate, but many of them are selected against because they interfere with the production of functional protein. Thus, genes are more "evolutionarily conserved" than are introns and "spacers." They can still change, however--often with no effect on the protein.

Changes in gene regulation, or in the sequences of "developmental control genes" can alter the way embryology proceeds, and can therefore produce plants or animals that are different in appearance, or that have different biochemical characteristics.

The former changes tend to be the ones that prevent DNA from different species from aligning properly at meiosis. Hence, interspecies hybrids are often sterile. The latter changes tend to be the ones that are responsible for the differences we can see in plants and animals, by which we identify them as different types. They are different types of mutations, with different types of consequences for the organisms, but they occur at roughly the same rates. Although they may occur at the same rates, they are not subject to the same kinds of selection pressures. Only DNA changes that affect the competitive success, and/or reproductive success of individual organisms are subject to selection.

[youngborean]

In genes themselves, changes occur at the same rate, but many of them are selected against because they interfere with the production of functional protein. Thus, genes are more "evolutionarily conserved" than are introns and "spacers." They can still change, however--often with no effect on the protein.

Changes in gene regulation, or in the sequences of "developmental control genes" can alter the way embryology proceeds, and can therefore produce plants or animals that are different in appearance, or that have different biochemical characteristics.

The former changes tend to be the ones that prevent DNA from different species from aligning properly at meiosis. Hence, interspecies hybrids are often sterile. The latter changes tend to be the ones that are responsible for the differences we can see in plants and animals, by which we identify them as different types. They are different types of mutations, with different types of consequences for the organisms, but they occur at roughly the same rates. Although they may occur at the same rates, they are not subject to the same kinds of selection pressures. Only DNA changes that affect the competitive success, and/or reproductive success of individual organisms are subject to selection.

So if I am to understand correctly, according to the definition of speciation I listed above, selection has No direct pressure on speciation. The mutations that cause meiosis to become screwed up are independent of the mutations that effect phenotype. So we would have to have a non-deteremental DNA mutations that effect Meiosis (which seem to be few and far between) existing in mating organisms who are well suited to overcome selection pressures. The former has no real reproducible beneficial mechanism, although translocation has become a beneficial labratory tool. The latter is well established as far as I'm concerned. There seems to be a really big degree of chance for this model (as a whole) to be considered established at this point in my mind. The issue that really gets me is that evidence for half of the model often seems to be the proof of the whole. Now I realize that the genetic information is there, so we are all left to postulate. But there are still major limitations in our data. I personally would argue that there are infinite limitations.

[Jose]

So if I am to understand correctly, according to the definition of speciation I listed above, selection has No direct pressure on speciation.

Well, since "speciation" is most accurately defined as "inability to produce fertile offspring," and is generally considered in the wild and not in the lab where we can play tricks, I think I'd have to say that this inference is incorrect (or at least too limited). If two bird species, such as eastern and western meadowlarks, never mate in the wild because their songs are different, then they are defined as species. This is true whether they could produce fertile offspring in the lab. At present, they look similar to us, but in time--because of the reproductive isolation--they will develop different characteristics.

Selection has played a role in this particular speciation event. Individual birds must recognize their species' mating songs, or they are selected against. Males whose songs are too different don't attract mates; females who do not recognize the common song don't find mates. There is, therefore, strong selection for the songs to be common within the population. At the same time, there are mutations. They can affect the wiring of the brain, and therefore the specifics of the song. Through genetic drift, a population's song can change--just not too fast. So, when two isolated populations, whose songs have drifted apart, come into contact, the selection for mating with birds with the "right" song maintains the species barrier.

Perhaps, in the lab, we could arrange conditions such that they would mate. We might get fertile offspring. By your definition, we would say they are variants of the same original species. But, in the wild, they don't mate. Therefore, mutations will occur over time, and the mutations will not be shared by the different "incipient" species. In time, mutations are likely to occur that affect the proteins that carry out meiosis, or there may be chromosomal rearrangements. If the two incipient species don't inter-breed, and don't "share" these mutations, then we will have complete reproductive isolation, fitting your definition of species.

In Real Life, it doesn't seem to matter what the initial barrier is to interbreeding between two populations of a species. It may be physical separation, or the development of a new food preference, or anything that creates two (or more) subgroups that don't interbreed. Once this happens, mutations cannot be shared between groups, and, eventually, mutations are bound to occur in genes that are critical for meiosis or embryonic development or sperm-egg recognition--and the populations (now species) are separated forever. More differences will accumulate with time.

The mutations that cause meiosis to become screwed up are independent of the mutations that effect phenotype.

Strictly speaking, screwed-up meiosis is part of the phenotype. Meiotic mutants are well known; their phenotype includes not only sloppy meiosis and therefore lowered fertility, but in many cases also increased sensitivity to UV light or other DNA-damaging agents. Such mutations are normally selected against, as you might imagine.

However, these mutations within species are not the same as meiotic incompatibilities between species. Between-species incompatibilities can be a result of slight changes in the proteins that run the process of meiosis, such that protein-protein complexes cannot form correctly. They can also include the sorts of chromosomal rearrangements we've already discussed. If one species has acquired a translocation between two chromosomes, but the other has not, then meiosis will result in gametes that have a deficiency or an excess of the genes that that have been translocated. Meiotic segregation typically pulls the centromeres apart, dragging with them whatever genes are attached.

So we would have to have a non-deteremental DNA mutations that effect Meiosis (which seem to be few and far between) existing in mating organisms who are well suited to overcome selection pressures.

Chromosomal rearrangements are DNA mutations. As long as there are no alterations of genes or gene expression at the breakpoints, then there is no reason to select for or against such rearrangements (except for meiotic segregation of genes inappropriately--which can be accommodated under the right conditions). Thus, these kinds of mutations can become fixed in a population, and thereby produce a barrier to reproductive success with closely-related populations.

Actually, mutations that affect meiosis are as frequent as mutations that affect any other trait. It's just that they are selected against quite strongly.

But, what we're talking about in inter-species hybrids is not mutations that affect meiosis, but the incompatibility of the chromosomes and gene products from the two parents. I've mentioned translocations and protein-protein complexes as two kinds of incompatibilities. The incompatibility results from putting the two different species' genomes together into a hybrid, rather than from "mutations" in the hybrid itself. How would the two species become different in the first place? By the relatively slow accumulation of mutations independently in each population. A little change here, another little change there, and the two populations drift apart genetically.

There seems to be a really big degree of chance for this model (as a whole) to be considered established at this point in my mind.

Yep. There's a lot of chance involved. That's why it's so slow--and why geneticists can make it go faster in the laboratory, and breeders can make it go faster in breeding programs. The geneticist can make choices as to which parents to use to create the offspring that combine the right traits; nature can't make this choice consciously. But just because chance is involved doesn't mean it can't happen. It just means that if we did it over again, it would not come out the same.

The issue that really gets me is that evidence for half of the model often seems to be the proof of the whole. Now I realize that the genetic information is there, so we are all left to postulate. But there are still major limitations in our data. I personally would argue that there are infinite limitations.

All that is "missing" is the specific lineage of mutations that occurred over several million years to account for a greater-than-species-level divergence. For every step in the process, there are "proof of principle" examples. Each bit can, and has, happened. Admittedly, this is not "proof" of the specific lineage of living things that we now observe--nor does anyone claim that it is.

Creationists like to claim that scientists claim that it is absolute proof, and thereby declare that scientists are lying to the public. They believe in absolute truth, and mistakenly assume that scientists claim they have absolute truth. Scientists do not have absolute truth, and never have, and never will. All we have is the data that are currently available, and the best explanations we can offer at the time.

We have proof of principle of each of the necessary steps. We have DNA sequence data that link all living things into a single family tree--just as we have DNA sequence data from individuals within known families that link them into a family tree. We have proof that species reproduce according their kind, and we have proof that mutations occur. We have proof that mutations affect phenotypes to greater or lesser degree. We have proof that some mutations are selected for, and others are selected against. We have proof of a variety of reproductive barriers between similar species. We have proof that slightly-different proteins (due to minor mutations) can fail to form fully-functional protein-protein complexes, and proof that chromosomal rearrangements can cause meiotic failures.

An analogy, albeit on a smaller scale, is finding a new type of tree that you have never seen before. It has seed pods. Is it fair to infer, from the "proof of principle" from trees that you do know, that planting these seeds will result in the growth of new trees of the new type? In this example, you are taking things you know, and applying them to something different, but for which the known principles apply. The only difference is that you can do the exact experiment to test your hypothesis. With evolution, we can't do that because it takes too long, and because a fundamental aspect of the mechanism is that it has no goal, and will not produce the identical results twice.