Faith writes:
Faith writes:
Faith writes:
It's just a variation on the same theme. Subpopulations merely differ from one another because of having different frequencies of alleles from other populations of the same species/kind due to reproductive isolation from the other groups for one reason or another*. Why is this treated as something special? The accidents AND selectively determined incidents of reproductive separation predictably produce new phenotypes by shuffling the alleles at the very least, often reducing the genetic possibilities too. Nothing is necessarily added in order for this to occur. Same situation as in the OP really**, with somewhat different reasons for the variations.
---------------
*"One reason or another" could be natural selection or geographical isolation or bottleneck or anything of that sort.
TimChase writes:
Well, what is neat about it is the fact that it demonstrates speciation in action in a way that in a certain sense is frozen in time, so that any time one visits the place, one can see the living evidence.
Faith writes:
But evidence of what? Of that fact that species vary phenotypically, sometimes to extremes? This is commonplace. The process that brings it about is the subtractive process under discussion which gives the lie to the idea that the ordinary processes of variation and selection demonstrate evolution.
1. Who says that your so-called "subtractive process" of is the only thing under discussion? I brought up ring species int the context of phenotypic variation -- in response to the original essay. As for the "subtractive process under discussion which gives lie" to anything, this is simply your unsupported assertion. However, one sentence later you mention "variation" which as you know is the result of mutation -- or what you would call the "additive process."
2. Mutations are quite common, even harmless ones. In fact they are so common that we will be using them to trace the lineage of cells in embryonic and oncological development:
The following story is about the tracking of accumulated,
harmless mutations (much as is done in the creation of phylogenetic
trees for species, e.g., the presence of the same pseudo-genes in both
chimps and humans) in the development of an organism as cells become
specialized. The story considers how this may be useful in the realm
of medicine, but I believe it will prove useful in evolutionary
developmental biology as well. Looks like cross-fertilization going
in both directions...
UPI: Scientists develop new analytical method
Top News, Latest headlines, Latest News, World News & U.S News - UPI.comTop News, Latest headlines, Latest News, World News & U.S News - UPI.com
Faith writes:
TimChase writes:
Wipe out that which connects the two extremes and they are no longer members of the same species -- but are they members of the same species while the bridge exists? Well, yes and no. Is cyan blue or is it green? At this point, we are asking the wrong question.
That's not a question I'm asking.
If you were concerned with how speciation takes place, it would be.
Faith writes:
TimChase writes:
Additionally, oftentimes those who deny the reality of macroevolution will do so at the level of species, claiming that one species cannot evolve into two. Or maybe they pick a somewhat higher level, such as denying that an autocatalytic RNA strand (essentially, a viroid with the ability to reproduce) could ever evolve into a human being. But once one admits speciation, the rest is largely just a matter of degree.
So goes the theory, but if the processes that bring about speciation simultaneously reduce the genetic diversity that evolution requires (beyond the mere variation on given genetic allotments), and mutation turns out not to be a sufficiently effective counter to this subtraction process, then this theory of an open-ended evolution is falsified.
3. From the above paragraph, "if the processes that bring about speciation reduce the genetic diversity...
and mutation turns out not to be a sufficiently effective counter to this subtraction process, ... then this theory ... of ... evolution is falsified." Yes. "If" such conditions were true, "then" this "open-ended" evolution
would be falsified. That is science. In contrast to pseudo-science which typically fails to make any predictions, science makes predictions and
is falsifiable. But being falsifiable is not the same thing as being falsified. Real empirical science is based upon the the evidence, and it stands or falls with the evidence.
Faith writes:
TimChase writes:
As for the generation of "new information," this is something which occurs principally in terms of the populations. For example, a single nucleic polymorphism ("snip") will result in a new allele, one which didn't exist in the population before -- and that is the generation of new information, but simply noise until it passes through the filter of natural selection into the general population.
This is a side issue but presumably even a deleterious allele could be selected, because of its association with others, no? The perennial question of course is How often is this process of the production of new alleles of any benefit? And, one I've asked before here that I don't believe has yet been answered, How do you KNOW a "new allele" "didn't exist in the population before?" How do you know it is not a rarely occurring event that has always been part of the genetic picture of this species?
4. Faith asked, "How do you KNOW a 'new allele' 'didn't exist in the population before?'." We know that there will be new alleles and or genes because mutations occur. We also know that there are oftentimes new alleles by observing new traits which did not exist in the population before. Moreover, we are developing the ability to trace these new traits to specific genes. Nothing particularly puzzling about this except for those who insist on being puzzled.
5. Faith asks, "This is a side issue but presumably even a deleterious allele could be selected, because of its association with others, no?"
Sometimes alleles are associated.
"If two alleles were found together in organisms more often than would be expected by normal inheritance patterns, the alleles are in disequilibrium. Disequilibrium can be the result of physical proximity of the genes. Or, it can be maintained by natural selection if some combinations of alleles work better as a team."
EVOLUTION
Excerpted from C. Colby
Page Not Found | University of Arkansas
You may also wish to look at:
Beneficial Mutations, Hitchhiking and the Evolution of Mutation Rates in Sexual Populations
Toby Johnson
Beneficial Mutations, Hitchhiking and the Evolution of Mutation Rates in Sexual Populations | Genetics | Oxford Academic
If a deleterious allele is associated with a beneficial allele, then it is the net effect of the two alleles together which is significant. Is it on the whole beneficial or deleterious? By how much? Beneficial mutations will tend to be selected for in ( 2/s) ln(2N) generations. The smaller the population, the more likely somewhat harmful mutations will become fixed in the population, and the more likely genetic drift will occur.
But the "selection" or fixation of deleterious mutations by themselves is far less likely than that of neutral mutations, and the fixation of neutral mutations is far less likely than that of beneficial mutations -- which, given their beneficial nature should become fixed in a population through natural selection much more rapidly than neutral mutations would become fixed simply as the result of genetic drift. Beneficial mutations "benefit" the organism, making it more likely that the organism will survive, reproduce, and thereby pass on those mutations to future generations, facilitating their spread through the population. In any case, this would be the subject of a course in Population Genetics.
For a quick overview, you might look at:
Lecture Summary 31 January 2001: Neutral Theory (I) and effective population size
Summary January 31 2001
For simulations, you might look at:
Population Biology Simulations
http://darwin.eeb.uconn.edu/simulations/simulations.html
For something more thorough, you might look at:
"Theoretical Evolutionary Genetics" by Joseph Felsenstein
http://evolution.gs.washington.edu/pgbook/pgbook.pdf
6. Faith asks, "The perennial question of course is How often is this process of the production of new alleles of any benefit?"
If one is looking for a rate of the production of new, beneficial alleles, this will involve a number of "problems." No doubt you are aware of neutral mutations -- these are silent mutations -- which get expressed the same way as the original alleles. But there are also effectively neutral mutations. These mutations are mutations which might actually be considered beneficial or detrimental to a small degree -- when compared to the allele that they are a mutation of. But their benefit or detriment is negligible enough to get eliminated from the population -- much like the alternate alleles which already exist and have persisted in the population for some time. Their effects are small enough that their beneficial or detrimental effect upon the survival of the organism becomes "washed out" by the genetic drift of the populations of other alleles for other genes, by the intermixing due to sexual reproduction, etc.. This is what maintains genetic diversity in a given population. Moreover, the smaller the population, the greater the benefit or detriment which is properly regarded as effectively neutral. The standard equation is 1/2>SN where N is the effective population size (i.e., a norm of the multigenerational population sizes) and S is the selection coefficient. So paradoxically, the smaller the population, the greater the number of alternate alleles which may be regarded as effectively neutral. Thus if a large population is reduced to a smaller size population, the effects of drift become more important. But the drift itself of some alleles for some genes will form part of the context around which other alleles for other genes are regarded as beneficial, detrimental, or effectively neutral. Then if the population grows back to its original size, many of those alleles will no longer be effectively neutral, but given the interdependence of alleles at different genes and the earlier drift, the new optima may be quite different.
How important is genetic drift to evolution?
http://www.uleth.ca/bio/bio3300/12.pdf
Fixation of New Mutations in Small Populations
Michael C. Whitlock and Reinhard Brger
http://homepage.univie.ac.at/...uerger/04WhitlockBuerger.pdf
A historically important paper is:
Model of Effectively Neutral Mutations in Which Selective Constraint is Incorporated
Motoo Kimura
PNAS | July 1, 1979 | vol. 76 | no. 7 | 3440-3444
Just a moment...
In one of the more technical articles, I found this interesting quote:
"A similar effect, but even more pronounced, is seen in this same population among the clones sampled in generations 5,000 and later. A clade comprising 70% of the clones at generation 5,000 was no longer seen in generations 8,000 and 10,000. This phenomenon, in which the dominant clade at some later time emerges from outside (rather than within) an earlier majority type, indicates a 'leapfrog' event; such events often can occur in large asexual populations that produce two or more competing beneficial mutations (12). These data therefore also suggest that many beneficial mutations appeared and achieved temporary success, but were not retained by natural selection over the long term in the face of other, even better mutations."
Genomic evolution during a 10,000-generation experiment with bacteria
NCBI
Similarly, if one were looking for the rate of production of either beneficial alleles (where the benefit was judged relative to other alleles for the same gene and one neglected the effects of alleles for other genes), this would be a mistake, as some alleles and genes are hypermutative, or may become hypermutative when exposed to certain proteins. For a very important example of this, there is the phenomena of hypermutation by which our B cells (part of the immune system) adapt to new pathogens. See:
Researchers Uncover Secrets of Immune System’s Munitions Factory
August 26, 2004
Researchers Uncover Secrets of Immune Systems Munitions Factory | HHMI
Selection and hypermutation seems to work rather well in the immune system, wouldn't you agree? Of course, when faced with a hypermutative pathogen such as HIV, things do turn out differently.
Faith writes:
TimChase writes:
However, the more interesting ways of generating new information consists of gene duplication, segmental duplication, chromosomal duplication, and polyploidy -- or the mutation of regulatory DNA which is responsible for determining when, where and how much a given gene gets expressed.
All these are varieties of mutation, right? And the same questions apply. How many are of any real use to the species as opposed to a disease process? How do you know they are unique to the species?
7. Faith asks, "All these are varieties of mutation, right?" Yes -- different kinds of mutations. Faith says, "And the same questions apply." Well then, the same answers would apply. However, in gene duplication, chromosomal duplication and polyploidy, the effects may not be as harmful as segmental duplication within the same gene -- since the same proteins will be produced. Faith asks, "How many are of any real use to the species as opposed to a disease process?" This is largely an empirical question -- unlike pseudoscience, empirical science will sometimes run into those. As for their being "unique" to a species -- I am not exactly sure what you mean. Some of the same mutations will occur in distantly-related species, but oftentimes the same sort of phenotypic change will be the result of a different genetic change -- which is easily identified through genetic analysis. Additionally, while given the size of the genome, mutations are fairly common, having the very same single nucleic polymorphism should be much less common. Moreover, the likelihood of having a series of the same mutations showing up in two species simply as the result of chance decreases exponentially with the number of mutations which are the same, like rolling sixes a hundred times in a row, or winning the lotto five times in a row. Theoretically possible? Yes. Something which it would be reasonable to expect? Not at all.
Faith writes:
TimChase writes:
The duplications make possible sub-functionalization (which is responsible for the dichromatic vision of our ancestors becoming our own trichromatic vision) and neo-functionalization (which is responsible for an enzyme involved in digestion being co-opted for the coagulation of blood).
Again, what makes you so sure that these functions originated from novel events?
8. I assume you mean, if we find the same mutation in chimpanzees as we find in humans, how do we know that they didn't occur as the result of two separate mutations in the two separate species, rather than as one mutation in one ancestral species? Well, if we are talking about insertions at the same relative point, these would be highly unlikely -- given the size of the genome. Similiarly, if we are talking about the single nucleic replacement of a large number of base pairs, this would be unlikely -- like rolling a large number of sixes in a row.
Faith writes:
TimChase writes:
And the mutation of regulatory DNA? A great deal more, evidentally. 99% of our 25,000 genes are homologous to the 25,000 genes found in mice. 96% of those genes are in the same exact relative order. So it would seem that the majority of evolution does not occur as the result of mutations in the genes themselves but in terms of the DNA which regulates gene expression.
Such similarities are just as well explained by similarities of design as by evolution. Probably at least 99% of a Toyota has parts of the same basic function as those in a Ferrari.
9. I should go ahead and cite a source for that figure:
Mouse genome mutation and selection
Mouse genome mutation and selection
The toyota-ferrari comparison is a poor one -- since silent mutations of strictly homologous alleles for the same gene will have occured less often in more closely related species -- and, to the extent that the rate of mutation is held constant, one will be able to measure the time since various species have separated. This will form a pattern which will hold for a very large number of genes which taken together constitutes a very large body of molecular evidence for evolution. The likelihood of this pattern of silent differences in alleles being the same without the species being related decreases exponentially with the size and number of alleles which one samples. However, my chief reason for introducing the mouse/human comparison was to point out those who are interested in understanding how evolution works rather than those who work in the interest of not understanding it.
For those who wish to understand, it is important to realize that much of the change which occurs due to evolution occurs not in the genes themselves, but in the regulatory DNA -- which contains more than double the amount of DNA found in the genes (3.5% regulatory, 1.5% in the genes). Regulatory DNA results in low fidelity, high redundancy networks of proteins with a great deal of plasticity.
Faith writes:
TimChase writes:
In any case, mutations take time. Natural selection will reduce the genetic diversity for a while when there exist strong selective pressures, but then new mutations will occur within the population, replentishing its genetic diversity.
So I've heard. But I haven't seen that this actually occurs, it is merely asserted to be the case. A lot is assumed here but not demonstrated.
10. So you say, but you could try looking up a few of the scientific resources yourself as opposed to visiting creationist websites.
Faith writes:
TimChase writes:
Moreover, once the two populations have been separated (for whatever reason), the mutations which occur in one population will no longer be communicated to the other population. The two populations will diverge, then tend to adapt to different environments and different pressures.
Yes, again, so goes the theory. But even without mutation, with the given complement of alleles taken from the parent population, a great deal of divergent changes are not only likely but inevitable. The adaptations, the selection, all the processes work the same way without mutations being assumed. Again, how do you know that any beneficial mutations ARE mutations, that is, how do you know they are novel events rather than predictable events that occur normally and repeatedly in the population?
11. See above, particularly (6), (8) and (9).
Faith writes:
Faith writes:
TimChase writes:
At some point, even if the two species come into contact with one-another, they will no longer be able to produce fertile offspring -- and they will continue to diverge. Quite simple, actually.
Yes, but the fact that they become unable to interbreed is simply a definitional point for evolutionists, though it doesn't in itself demonstrate anything except that a species may vary to the point that interbreeding becomes difficult to impossible. The Kinds were designed to vary enormously and the loss of the ability to interbreed would tend to preserve the varieties.
12. Hardly definitional -- as it results in reproductive isolation, then drift and mutation will result in quite different sets of alleles over time. As for "kinds," how large were the kinds? Would mice and humans together form a kind? If you attempt to keep chimpanzees and humans separate, simply on the basis of genetic similarity, you are going to either have widely varying species which are far less similar genetically than humans and chimps, or you are going to have a very large number of kinds. Humans are more closely related (at least genetically) to chimps than chimps are to apes. What of foxes, wolves, and dogs? Mules, horses, and zebras? Lions, tigers and leopards? Separate kinds?
Faith writes:
TimChase writes:
Of course, if you are looking for really good smoking guns as far as demonstrating the reality of evolution, some of the best I am aware of are pseudogenes and endogenous retroviruses. Not exactly what you would call conclusive -- nothing is in empirical science. As Duhem's thesis shows, it is always possible for someone to choose a less reasonable interpretation of the empirical evidence over a more reasonable interpretation -- indeed, one can coherently maintain that the world is only five minutes or five seconds old without fear of self-contradiction. But for the good majority of people who understand what they are and how common they are, I suspect pseudogenes and ERVs would be enough. (Additionally, I am rather fond of the idea of having 30,000 retroviruses in every one of my haploid genomes -- quite a collection!, or the idea that nearly fifty percent of my genome appears to be retroviral in origin [e.g., consists of retroelements].)
All this is off topic but maybe you could start a new thread for it.
13. Perhaps. At the same time, pseudogenes help to illustrate an important point: a potentially deleterious mutation may be relatively insignificant given the right environment. For example, most mammals are able to produce their own vitamin C. Chimps and humans are not able to do so because, while they have the gene for the production of vitamin C, it has mutated. It could mutate because we had other sources of vitamin C. Interestingly, the mutations in the gene were identical in both humans and chimps.
14. Similarly, retroviruses are important because they originally introduced retroelements which make retrotranspositions of segments and genes possible (i.e., retrotransposons) -- that is, duplications of the genes and DNA segments in genomes. DNA viruses evidently introduced transposons which cut and then insert genes and segments. And interestingly, while endogenous retroviruses oftentimes reproduce simply for their own sake (serving no function as far as the organism in whom's genome they are embedded in is concerned), they do produce nice phylogenetic trees -- particularly when one takes into account the fact that they share the same insertion points between species.
This message has been edited by TimChase, 12-08-2005 01:30 PM
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