Where's the evidence *against* evolution?

[DrFidelius]

but that brings up another point. so much of what people have been referring to in this thread about ‘genetic mutations’ is actually an inherited trait caused by a mutation many generations ago.

What point is that? Most evolutionary change is the result of the shuffling of existing alleles in a population rather than the introduction of new mutations.

Random neutral mutations provide the potential for changes in a population. When the environment changes, there is the possibility that a formerly neutral variant will now be exposed to selection pressure. A mutation in an individual is as trivial as a single grain of sand on a beach. It is only if that variation in the genetic material has spread through a population (or sub-population) that it can become significant for descent with modification.

[wolfman]

sorry for the continued hijack, but I wanted to clarify.
Andros, like I said I’m being devil’s advocate, but my post was primarily in response to your request for posting “real, scientific evidence supporting creationism”
The whole concept is a oxymoron and pointless.
A creationist(or even a solipsist for that matter) can attack evolution on its own grounds. You can’t scientifically support creationism, but you can scientifically argue with evolutionism, becuase it is just one theory which fits the evidence. Which I guess was my main point. Scientific principles change radically over time. Evolutionists take any counter theory to evolution as a support of creationism. I have no doubt that there are many flawed theories is evolution, and most every other known science. The one thing we have proven in history is that we don’t really know shit.
I don’t explain myself very well but let me try to sum up.
Overwhelming confidence in current theory of evolution isn’t scientific, its highly unlikely that we “nailed it the first time” However confidence that there is a scientific explaination of how we got here rather than a faith based one is scientific.

[JonF]

wolfman I think all of your points have been adequately addressed, except:

Creationism isn’t supposed to be able to be proven scientifically, thats why it’s called having faith.

There are many people who believe in divine creation for reasons of faith. I do not share that belief. I (and, I think, most scientists) do not try to change those people’s minds and do not denigrate their belief. Many scientists share that belief.

However, there are people who claim that there is such a thing as “creation science” which is scientifically founded and based on evidence and facts. These people want “creation science” taught in schools, alongside or instead of evolution. Their claims have been tried in the “court” of science and in courts of law and have been found wanting. This has not discouraged them. Those people do claim that creationism is supposed to be, and is, provable scientifically. For an extensive list of links to sites of such people, see http://talkorigins.org/origins/other-links.html#creationism .

Plus the fact any scientist who is personally offended by the thought that creationism could be right, isn’t a very good scientist.

I would agree if you had said “divine creation” instead of “creationism”. “Creationism” can be interpreted as several things, including so-called “creation science”. I believe (and can support if challenged) that all scientists should be professionally and personally offended by the ludicrous claims, bad science, and slimy tactics of almost all “creation scientists”. Calling them scientists and calling what they do science is an insult to real science and scientists.

[Mauve_Dog]

*Originally posted by wolfman *
**I don’t explain myself very well but let me try to sum up.
Overwhelming confidence in current theory of evolution isn’t scientific, its highly unlikely that we “nailed it the first time” However confidence that there is a scientific explaination of how we got here rather than a faith based one is scientific. **

We didn’t nail it the first time. Ever hear of Spontaneous Generation? Or Lamarckism? These are but two previous attempts at explaining how evolution works. Both have been discarded as ‘unsatisfactory.’ The current working model of the Modern Synthesis is the best thing going. If there’s overwhelming confidence in the theory, it’s because it serves as the current best explanation for what we observe. As we learn more, the theory will be adjusted. I seriously doubt, however, that there will be some monumental finding that will result in an utter dismissal of evolution in favor of creationism.

[tracer]

KeithB wrote:

There are a group of people in Italy, all descended from the same person, who do not get hardening of the arteries. They can eat all the fatty foods they want, and not get that form of heart disease. Which is a good thing for an Italian! 8^)

Does this count as a beneficial mutation?

Two questions:

1. Has anybody isolated the chemical compounds responsible for the lack of hardening of the arteries within this group? And

2. Can I get some?

[Triskadecamus]

OK, suppose there were slime critters in the shallows of an inland sea, in the supercontinent that existed before Pangea. Now suppose that slime critters mostly eat the dead cells of algae, and in the course of foraging for it they ingest diatoms, which they cannot digest. What with the climate and all, life is good for slime critters everywhere, and their numbers begin to increase.

After a million years or so, there are millions of descendants of each slime critter, and many are spread out over vast distances from the original slime critters, of a million years ago. All the slime critters are about the same, of course, and their diet is more or less the same. Among the many billions of slime critters, though are some which have normal gene for a narrowing of the elimination orifice of those particular slime critters. The difference is inheritable, although does not express itself in all critters with the allele for inheritance. This characteristic allows those particular slime critters to retain and utilize the bodies of diatoms to improve the sifting of seawater to obtain algae. Since the smaller orifice tends to limit the expulsion of spore sacks during reproduction, it is not entirely beneficial, since it causes a decrease in the number of offspring in some individuals. On the whole, it is neither beneficial nor baneful.

Another million years go by, and things change a bit. Now there is a lot more competition for dead algae. In addition, there are scavengers swimming around eating slime critter spores. The differences make the population of slime critters fluctuate a bit. High population levels tend to make small spore sacs a slightly less detrimental characteristic, since the spore eaters will eat either size entirely. Low algae populations make the sifting benefit more beneficial. The entire population begins to experience a shift in genetic background as the small portion with the expressed allele begins to have a better chance of passing on their genes. During the next million years the inland sea begins to dry out. Many areas of the inland sea are much as they were two million years ago, but in some areas the balance changes. After the end of the third million years the slime critters in various areas have developed differently. In some areas small orifices are almost unknown, in others they are almost universal, in still others, the diversity includes both types.

When predators that cannot digest the diatom bodies are introduced into the environment in one location, all the original types of slime critters are eliminated in only a few hundred thousand years. The predators gradually stop preying on slime critters when all those which do so die of gastric blockage. In that location the change is irreversible, since all the slime critters in the environment have the allele for narrow orifices. Elsewhere, the original genome still exists, and might develop in other ways.

So one genetic difference and external changes can create three or more different populations of one species. That is the basis of speciation for these imaginary critters. So the count of how many mutations might have occurred during that same three million years would be meaningless. When all slime critters become extinct during the collision of Pangea, it all becomes a dead end. Arithmetic is not going to provide us with much meaningful guidance.

Tris

[APB9999]

MauveDog:
I don’t seem to be getting my point across. First, it is impossible to describe a mutation as advantageous or not without considering the context in which the organism exists. But we CAN eliminate silent mutations and many lethal mutations (at least those that are lethal because the organism is not viable, we still miss those mutations that are lethal because of the environmental context). These are independent of the environment. So when we’ve accounted for these mutations, we can take the remainder as an absolute upper bound, as I said before, on the possible rates of beneficial mutations. This will be, I repeat, a gross overestimate.

Now IF we were to find that this MAXIMUM rate was TOO SLOW to account for the rate of evolution observed in the fossil record, what choice would there be but to step WAY back and start interpreting the evidence afresh?

All this is aside from the point of WOULD we find this to be the case. Obviously, we wouldn’t. But that’s not what the OP asked.

[Smeghead]

About counting mutations between me and E. coli: One very common way to figure out how organisms are related is to do just this with certain enzymes. For instance, cytochrome c is highly conserved - it mutates very slowly. So if you get a bunch of mammals, you can go through, pick out all the mutations that have occurred in the various lines, and piece together how the species are related and how long it’s been since they diverged.
As I said, this is usually done with just one or two genes, and usually works best with very highly conserved genes. If you were to look at a section of so-called “junk” DNA, mutations are happening so fast and furiously that putting together any relationships would be impossible. FWIW, I’m not aware of any genes that are so highly conserved that you could use them to compare us and E. coli.

About the supposed lack of positive mutations: Nobody goes to the doctor to complain that they’ve been feeling unusually healthy. There’s no money in researching drugs that allow unusually healthy people to get sick at a normal rate. Therefore, positive mutations will tend to slip by unnoticed, unless they’re searched for, as is the case with some of the examples posted here already.

tracer - if no one’s isolated the chemicals yet, I can guarantee there are dozens of drug companies working on it.

[Ben]

*Originally posted by jmullaney *
**

Izzy This is fairly simple. Figure out how many DNA bits there are in a human. Each bit has four possible values. Imagine them as blocks. Start with a pile of none, and add a random block. Keep adding random blocks or changing the ones that you have for the required number of steps to get the length. Then figure on a few more just to get the rest right. Remember too that 96% of our DNA is junk to begin with so don’t count that. And, you have to account for the fact that multiple mutations can happen at the same time. **

Uh, no. You’re forgetting that evolution doesn’t have to reinvent the wheel. Under your scheme, hemoglobins alpha, beta, eta., etc. all have to evolve through separate point mutations, when in reality they (like most genes) are the result of gene duplication.

Be aware that there are some studies that address Izzy’s question. Kimura, for example, did a famous study in which he calculated the # of mutations per generation, etc., etc., and found that it was so high that it should have killed everyone off. His (somewhat controversial) conclusion was that most mutations are neutral. It’s pretty obvious to me, as a structural biologist, that most mutations are neutral, so I’m not sure what the big deal was supposed to be.

If you want to know more, read the appropriate chapter on the Neutral Theory in Ridley’s Evolution.

-Ben

[Ben]

*Originally posted by APB9999 *
**
There is no smaller (nonsilent) mutation than the substitution of one nucleotide for another, causing substitution of one amino acid for another. Because natural selection has already created the genes we are carrying, and mutations occur randomly, any such mutation has a far smaller than 50% chance of being advantageous, on the face of it.

**

While to some extent you have a point, you’re forgetting about lag load. If we haven’t caught up with changes in the environment, then it’s more likely to have a mutation that will push us in the right direction.

The classic example is those fruits that were eaten by giant sloths or whatever (ok, so I don’t remember all the details.) They needed to be big so that giant sloths would eat them and disperse the seeds. Now that the sloths are extinct, the fruits are too big and they just plop to the ground and never get far from the tree. If a mutation affects the regulatory region of a gene for a growth hormone which controls fruit size, you could say that the mutation has a (roughly) 50/50 chance of being beneficial, because half the time it will make the fruits at least a little smaller. Admittedly, that’s only for mutations which hit the regulatory region.

-Ben

[David_B]

Wolfman said:

You can’t scientifically support creationism

I know that; you know that. Unfortunately, there’s a whole bunch o’ creationists out there who can’t seem to get it through their heads.

There have been other threads here about this topic. If somebody says, “I believe in creationism strictly on faith,” then we are in the turf you mention – we can’t argue with that scientifically.

However, if a creationist comes in here (as the often do) and starts making claims like, “I believe in creationism because the 2nd law of thermodynamics says evolution can’t be true, and besides, there isn’t enough dust on the moon for it to be as old as evolutionists say, and I’ve never seen a dog evolve into a cat!” THEN we can (and, I would say, must) use science to shoot down the claims.

[tracer]

What’s sad is, I remember reading a children’s book when I was a little boy, in which a whole bunch of dinosaurs were gathered around this one dinosaur egg watching it hatch, and it hatched into a bird. This was supposed to be a true representation of how the first birds evolved – one generation they were pterodactyls or apatosaurs or velociraptors, and the next, boom, they were full-fledged birds.

I’ve heard of punctuated equilibrium, but this is riduculous!

If I ever see that book again, I’ll take down its title and publisher info and write a nasty letter to the author.

[APB9999]

Hi Ben, I’m a structural biologist too! Let me try spelling out my reasoning a little more about why I reject the notion that a mutation will be beneficial with 50% probability.

Some of what follows is simplistic for brevity’s sake, but not in such a way as to affect my conclusions.

Take a gene. Focus on a single one of the residues coded for in that gene. Start with this residue being randomly chosen from the twenty amino acids; say it is X. Now mutate it and check to see if the molecule is better (leaving aside the details of what our metric for this judgement is). Again for brevity, let the probability of mutation to each of the other nineteen residues be equal. Since mutation is a random process, the likelihood of mutating to any specific residue is one in nineteen.

1. How likely is it that mutation away from X, to Y, is beneficial? Well, we chose X randomly, so if there is a change it ought to be (on average) as likely to improve the protein as to make it worse. This might be the origin of the 50/50 idea. So on average, about 9 or 10 of the residues will be improvements and 9 or 10 will be detrimental. The odds of both are 9.5 out of nineteen.

2. However, the residues in natural proteins (those residues that are not silent to the function of that protein) are never chosen at random. They are always under the pressure of natural selection.
   So let’s now assume that natural selection has acted on the residue, but has not completely optimized it, either because it hasn’t had time or because the environment has changed somehow. Otherwise ANY change is detrimental and the issue is moot.
   So there IS some possible improvement. Is the likelihood that a random change will be beneficial still 9.5 times out of 19 as above? No! It will of course be less than this because we’re already in the “top half” of residues.

This is a very simplified scheme, but I think it captures the essence of why I feel that most mutations are more likely to be detrimental than beneficial.

The only argument that negates this, that I see, is that if the environment has changed, previous optimizations are irrelevant. But of course you can see that’s too extreme. Conditions generally change more slowly than would negate ALL previous selection on a molecule. If they didn’t, we would more likely see extinction (of the gene, at least) than adaptation.

[Mauve_Dog]

*Originally posted by APB9999 *
**MauveDog:
I don’t seem to be getting my point across. First, it is impossible to describe a mutation as advantageous or not without considering the context in which the organism exists. But we CAN eliminate silent mutations and many lethal mutations (at least those that are lethal because the organism is not viable, we still miss those mutations that are lethal because of the environmental context). These are independent of the environment. So when we’ve accounted for these mutations, we can take the remainder as an absolute upper bound, as I said before, on the possible rates of beneficial mutations. This will be, I repeat, a gross overestimate.

Now IF we were to find that this MAXIMUM rate was TOO SLOW to account for the rate of evolution observed in the fossil record, what choice would there be but to step WAY back and start interpreting the evidence afresh?

All this is aside from the point of WOULD we find this to be the case. Obviously, we wouldn’t. But that’s not what the OP asked. **

I think I see where the confusion (at least my confusion) lies. There is a big step between molecular biology and rates of mutation (as expressed in # mutations / gamete / generation) and rates of evolution as seen in the fossil record. The basic assumption seems to be that the two are proportional. IF this is true, and IF we can calculate a theoretical maximum rate of mutation, and IF this theoretical maximum is too slow to account for the observed rate of speciation as seen in the fossil record, THEN what we probably need to do is re-evaluate our understanding of the linkage between molecular mutations and gross morphological change, not re-evaluate ‘evolution’ as a whole. Even if we scrapped everything we know about molecular biology, it would not invalidate the observed ‘large-scale’ processes of natural or sexual selection, for example. I apologize if I am being overly obtuse here, but I don’t see your scenario as being evidence against evolution.

[edwino]

I’m a molecular geneticist in training. My thesis actually deals with these eye “switch” genes which are incredibly conserved – Drosophila dachshund or eyeless mutants can be rescued by insertion of the human copies into the genome.

To add fuel to the fire, mechanisms of Gould’s punctuated equilibrium may be coming to light. This gives another dimension to the “estimating mutation rate” debate.

Much of our “junk DNA” is derived from what are called endogenous retroviruses. These are sequences of DNA which look like replication-defective retroviruses which have incorporated, gone germ-line, and stayed with the genome. Some of these have greater than 100,000 copies/genome.

A large scale retrovirus insertion can very rapidly interrupt scores of genes and alter other ones by changing promoter activity (making the genes expressed more or less). It also may promote large scale genome reorganization (deletion, duplication, translocation) as homologous (same) sequence is needed for recombination of DNA, usually.

Interestingly, a recent Nature article reports discovery of a gene called syncytin. This gene is contained in one of these endogenous retroviruses, HERV-W (which only has 7 or so copies in the genome). This is the first gene found to be expressed off of an endogenous retrovirus, and kind of redefines the concept of “junk DNA.”

Also, this is wonderful, because we may be able to see a type of macroevolution in action. Mice and many other placental mammals lack HERV, syncytin, and also lack a syncytial trophoblast (tissue around the placenta which interacts with the maternal blood stream). The formation of a syncytium (large polynucleated cells formed by cell fusion in this case) is also correlated with syncytin expression. Retroviruses in general tend to make syncytiums, possibly as a way of evading host defenses. The trophoblast in primates does exactly the same.

Mi, et. al. Nature 403, 785 - 789 (2000) Macmillan Publishers Ltd.

Hypothesis presented : Lateral transmission (inheritance of functional genes from other organisms or viruses) has occured in this instance in humans. This has never been seen at all. We can theorize that this probably has happened in other cases.

Sometimes viruses, upon excision, will take host DNA with them. If 2 species are afflicted with a viral infection, we can propose trans-species gene exchange through this mechanism. Of course, it would be rare, but what in evolution is not?

[edwino]

So, as a scientist and evolution believer and all, I’ve always wondered about evolution of the heart.

Think about it :

-The heart is formed from the curling of one tube. Through curling and partioning, it forms a working 4 chambered vessel. This partioning is accomplished by the migratory neural crest cells, which come from near the developing spine. At birth, through the change in differential pressures, blood flow basically reverses and it assumes a different function, as oxygenation is received from the lungs instead of the placenta.

-Evolution proposes that the heart evolved this way through gradual advantageous mutation, all the while maintaining physiologic function. Either that, or it evolved while having a different function (probably unlikely, as heart homeotic genes are quite highly conserved insect to vertebrate).

-All this happened after the chordate clade branched off. The primitive heart before this was probably just a beating tube (like insect hearts).

I know this is a gross oversimplification (and therefore must inherently lose some meaning), but if you take a primitive heart to be a 2 chambered deal, how do you propose to go to 3 chambered (like amphibians) while maintaining physiologic efficiency? It would have to be done really quickly with a huge modification, as I can’t think of a situation where inducing a partial bend/fold/partitioning of the tube would give more efficiency. It isn’t ruled out, though, but you would also need remodeling of the circulatory system, which may have another set of genes.

To add insult, it would have to be done again twice for 3->4 chambers for the mammalian lineage and perhaps for reptiles->birds.

If I were looking for intelligent design in nature, that would get my vote.

[jb_farley]

edwino,

very good argument. if forced to defend evolution, my only tack would be that mutations can happen which have a neutral effect, or relatively neutral. there are beneficial mutations, and maleficient, and some just plain swiss. or it could have been a disadvantage, but coupled with a strong advantageous mutation.

in both cases, the resultant offspring would probably tend to pass that odd heart structure to their offspring etc, and either the heart develops to a sufficiently complex degree at some long point down the line, or else the environment changes suddenly and a three- (and then four-) chambered heart becomes mightily advantageous.

am i spelling advantageous correctly?

[edwino]

jb_farley :

Point well taken. A strong selective advantage could outweigh temporary disadvantage. The problem that I see is that no organism up from fruit flies seems to be able to function well without a heart. Over a few generations, any such selective advantage would necessarily segregate away from the inefficient “heart transition-state”, and you’d be left with the old heart and a new selective advantage. Even if the two traits are tightly linked, let’s say 0.1 centiMorgans, you would still expect 1/1000 progeny to be a recombinant. In evolutionary terms, this is nothing.

If it was the same gene giving both the intermediate “heart transition-state” and the selective advantage (let’s say like Tay-Sachs heterozygotes’ decreased susceptibility to tuberculosis or sickle-cell disease and malaria), I believe a gene duplication event leaving the duplicated copy of the intermediate “heart transistion-state” gene able to stay the same, while the original locus recombines with the original heart gene to fall back to the same original heart. I suppose this is highly speculative, but all you need is one in a billion for this to have significant impact evolutionarily.

Off topic:
My current theory (I should save this for qualifying exams, really) is that heterozygote advantage is permanently endowed upon a population by gene duplication. CF, Tay-Sachs, sickle-cell dz and other common genetic disease can only be propogated in a population without the necessary disadvantage given by the homozygous indivuals in this way. Who’s to say…

[Ben]

Originally posted by Mauve Dog *
** The basic assumption seems to be that the two are proportional.*

Maybe ABP999 can help me out on this, but AFAIK they aren’t proportional. Most innovation in vertebrates is anatomical, and genetically happens in the timing of genes- there isn’t the sort of biochemical innovation you see in bacteria. As a result, if you look at a monophyletic rump like the birds, you see that a subset of reptiles can evolve very quickly anatomically, and still be quite similar genetically. So if you make a phylogenetic tree for vertebrates, birds come out being very similar to alligators. (Incidentally, it should be stressed that phylogenetic trees don’t arrange organisms on the basis of “similarity.” I find that fact to be amusing, because creationists spend so much time stressing that all phylogenetic trees are based on similarity and the assumption of a constant rate for a molecular clock, etc. etc. They have all these complex and detailed explanations of how phylogenetic trees are made and why the trees don’t work, but in reality their explanation has nothing to do with the real algorithms that are used in making the trees.)

-Ben

[betenoir]

ONCE AND FOR ALL, MUTATION PLAYS A VERY MINOR ROLE IN EVOLUTION.
Unless you count me as a mutation because I have my mother’s eyes and my father’s nose.
For multicelled creatures, natural selection is the driving force in evolution. Sex provides the variations, not mutation (except in rare cases.)