the phylogeographic challenge to creationism

You are confusing genetic diversity with phenotypic variation. What I am suggesting is that an increase in the second corresponds to a reduction in the first in most of the Evolutionary Processes. If I have time I may get back to the rest of your post tomorrow, but when the discussion gets bogged down with too many posters who are making this kind of mistake instead of making an honest effort to respect and understand what I'm saying I may not be up to it.

Do you understand what the word "phenotype" means? Why don't you define it for me. What is a phenotype? Because you don't seem to be using it correctly if you think that an increasing number of phenotypic variations represents a loss of genetic diversity. We can't understand what you're saying because you appear to be using words you don't understand. It's gibberish.

Where do we get phenotype variation from?As far as the rest of my post goes, please feel free to read it when you are able. I don't want you to feel ganged up upon, even though you and I have had this conversation before. You didn't answer me the last time I gave you this explanation so I thought I'd bring it up again. I linked to the thread where we talked about this before.This message has been edited by DBlevins, 11-27-2005 11:43 PM

We get it from SELECTION or ISOLATION or MIGRATION or BOTTLENECK or etc etc etc which is the whole thing I have been saying from the very beginning. Some genes go with the migrant or bottlenecked or selected population, and others are eliminated from the new population in this process. Usually, not always but usually. The overall result is a reduction in genetic diversity, in the very process of "speciation" or the development of new phenotypic expressions.Mick had no problem with this very simple statement. See his Message 29I have no idea why you and crashfrog have a problem with it, but it gets to the point that it is not worth trying to discuss it with you.This message has been edited by Faith, 11-28-2005 02:23 AM

See above post to DBlevins and Mick's Message 29This message has been edited by Faith, 11-28-2005 02:09 AM

Well, naturally - that's the crux of the debate Assuming each new offspring has a unique genetic make up, I'd disagree with you. Mutation comes first, and basically every offspring has mutations. If there is a case where there is no mutations, there is no evolution. We aren't talking about fish leaping out of the water here, we're basically talking about a gradual change in geographic location, each presenting slightly different challenges to survival so that at one end the population lives in forest land, and at the other it might live in mountainous regions. These two populations are seperated so they are reproductively isolated and so will evolve in different directions.Still, for the most part this turns out to be true - most populations do go extinct as the selection pressure becomes too great. Its possible, it just depends on the definition of macroevolution. If the definition of macroevolution is 'the point where type x loses its xness' or 'the point where organism x^* loses the characteristics which define it as organism x', then macroevolution does not occur. This definition, however, would not be a definition agreed on by evolutionists.A better, yet still incomplete, definition might be 'macroevolution occurs when organism x^* develops a novel characteristic which sets it apart from other organisms'. Unfortunately this will inevitably subsume over into microevolution so in short, macroevolution is a subjective rather than an objective classification. Given that mutation is an essential, nay integral, aspect of the Theory of Evolution, are you surprised? That's like criticising the Theory of Gravity by saying 'The curvature of space/time appears to be the only hope for cosmic scale gravity'Fecundity doesn't, by itself, increase genetic diversity. Fecundity, the fact that each offspring is a unique mutant⁺, and the fact that not all offspring succesfully mate leads to a change in allelle frequency in the population. If the population is successful it might increase in size, and given the unique organism 'principle' this is an increase in genetic diversity since there are now more unique genotypes in the population. Indeed, just pointing out that mutations to the DNA sequence is not the only way to elicit change in populations, and that epigentics can create measurable changes to the phenotype within one generation.^* More accurately: a population of organism x
⁺ I'm principally discussing sexual reproduction.

I'm bumping this because Faith ignored these examples where genetic diversity did NOT decrease as a consequence of speciation since it occurred in sympatry...and not to pick on Faith, nobody else picked up on these examples either Ok, here come the cichlids,
Note, going from the arguement in the OP, why do cichlids form populations/species that no longer exchange genetic information with one another even though the populations occur in the same lakes i.e. sympatric speciation? This is a nice example of macroevolution that is observable at the genetic level...what is the difference between what we observe between cichlid species as opposed to within cichlid populations? (Note: most of these articles are open access and anyone who want to, can read them)quote:
--------------------------------------------------------------------------------
BMC Evol Biol. 2005 Feb 21;5(1):17. Related Articles, Links
Out of Tanganyika: genesis, explosive speciation, key-innovations and phylogeography of the haplochromine cichlid fishes.Salzburger W, Mack T, Verheyen E, Meyer A.Lehrstuhl fur Zoologie und Evolutionsbiologie, Department of Biology, University of Konstanz, 78467 Konstanz, Germany. walter.salzburger@uni-konstanz.deBACKGROUND: The adaptive radiations of cichlid fishes in East Africa are well known for their spectacular diversity and their astonishingly fast rates of speciation. About 80% of all 2,500 cichlid species in East Africa, and virtually all cichlid species from Lakes Victoria (approximately 500 species) and Malawi (approximately 1,000 species) are haplochromines. Here, we present the most extensive phylogenetic and phylogeographic analysis so far that includes about 100 species and is based on about 2,000 bp of the mitochondrial DNA. RESULTS: Our analyses revealed that all haplochromine lineages are ultimately derived from Lake Tanganyika endemics. We find that the three most ancestral lineages of the haplochromines sensu lato are relatively species poor, albeit widely distributed in Africa, whereas a fourth newly defined lineage - the 'modern haplochromines' - contains an unparalleled diversity that makes up more than 7% of the worlds' approximately 25,000 teleost species. The modern haplochromines' ancestor, most likely a riverine generalist, repeatedly gave rise to similar ecomorphs now found in several of the species flocks. Also, the Tanganyikan Tropheini are derived from that riverine ancestor suggesting that they successfully re-colonized Lake Tanganyika and speciated in parallel to an already established cichlid adaptive radiation. In contrast to most other known examples of adaptive radiations, these generalist ancestors were derived from highly diverse and specialized endemics from Lake Tanganyika. A reconstruction of life-history traits revealed that in an ancestral lineage leading to the modern haplochromines the characteristic egg-spots on anal fins of male individuals evolved. CONCLUSION: We conclude that Lake Tanganyika is the geographic and genetic cradle of all haplochromine lineages. In the ancestors of the replicate adaptive radiations of the 'modern haplochromines', behavioral (maternal mouthbrooding), morphological (egg-spots) and sexually selected (color polymorphism) key-innovations arose. These might be - together with the ecological opportunity that the habitat diversity of the large lakes provides - responsible for their evolutionary success and their propensity for explosive speciation.--------------------------------------------------------------------------------more references,Baric S, Salzburger W, Sturmbauer C.
Phylogeography and evolution of the Tanganyikan cichlid genus Tropheus based upon mitochondrial DNA sequences.
J Mol Evol. 2003 Jan;56(1):54-68.Ruber L, Verheyen E, Meyer A.
Replicated evolution of trophic specializations in an endemic cichlid fish lineage from Lake Tanganyika.
Proc Natl Acad Sci U S A. 1999 Aug 31;96(18):10230-5.Here are some bat references,quote:
--------------------------------------------------------------------------------
Mol Phylogenet Evol. 2004 Dec;33(3):764-81. Related Articles, Links
Phylogeny and phylogeography of Old World fruit bats in the Cynopterus brachyotis complex.Campbell P, Schneider CJ, Adnan AM, Zubaid A, Kunz TH.Department of Biology, Boston University, Boston, MA 02215, USA. pollyc@bu.eduTaxonomic relationships within the Old World fruit bat genus, Cynopterus, have been equivocal for the better part of a century. While nomenclature has been revised multiple times on the basis of phenotypic characters, evolutionary relationships among taxa representing the entire geographic range of the genus have not been determined. We used mitochondrial DNA sequence data to infer phylogenetic relationships among the three most broadly distributed members of the genus: C. brachyotis, C. horsfieldi, and C. sphinx, and to assess whether C. brachyotis represents a single widespread species, or a complex of distinct lineages. Results clearly indicate that C. brachyotis is a complex of lineages. C. sphinx and C. horsfieldi haplotypes formed monophyletic groups nested within the C. brachyotis species complex. We identified six divergent mitochondrial lineages that are currently referred to C. brachyotis. Lineages from India, Myanmar, Sulawesi, and the Philippines are geographically well-defined, while in Malaysia two lineages, designated Sunda and Forest, are broadly sympatric and may be ecologically distinct. Demographic analyses of the Sunda and Forest lineages suggest strikingly different population histories, including a recent and rapid range expansion in the Sunda lineage, possibly associated with changes in sea levels during the Pleistocene. The resolution of the taxonomic issues raised in this study awaits combined analysis of morphometric characters and molecular data. However, since both the Indian and Malaysian Forest C. brachyotis lineages are apparently ecologically restricted to increasingly fragmented forest habitat, we suggest that reevaluation of the conservation status of populations in these regions should be an immediate goal.--------------------------------------------------------------------------------more references
Pestano J, Brown RP, Suarez NM, Fajardo S. Related Articles, Links
Phylogeography of pipistrelle-like bats within the Canary Islands, based on mtDNA sequences.
Mol Phylogenet Evol. 2003 Jan;26(1):56-63.Ditchfield AD. Related Articles, Links
The comparative phylogeography of neotropical mammals: patterns of intraspecific mitochondrial DNA variation among bats contrasted to nonvolant small mammals.
Mol Ecol. 2000 Sep;9(9):1307-18.This message has been edited by Mammuthus, 11-28-2005 03:50 AM

quote:

---

This occurs in all the forms of "evolutionary processes." It occurs in natural selection and it occurs in artificial selection (breeding), it occurs for geographic reasons and it occurs for behavioral reasons etc. etc. etc. It occurs wherever a part of a gene pool is isolated reproductively from the larger gene pool, in any way whatever and for any reason whatever, by removing some genetic potentials and bringing new genetic combinations to phenotypic expression that were suppressed in the parent population with its greater genetic variability.

---

This is false. The genetic combinations and their consequent phenotypic expression are not "suppressed" in the parent population at all. They may occur at a low frequency but that has nothing to do with suppression...evolution without mutation is also false and there are plenty of enzymatic and population studies to back this up.For example, here is the diversification of bacteria over 10 K generations.

quote:

---

Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3807-12. Related Articles, Links

​

Genomic evolution during a 10,000-generation experiment with bacteria.

​

Papadopoulos D, Schneider D, Meier-Eiss J, Arber W, Lenski RE, Blot M.

​

Abteilung Mikrobiologie, Biozentrum, CH-4056 Basel, Switzerland.

​

Molecular methods are used widely to measure genetic diversity within populations and determine relationships among species. However, it is difficult to observe genomic evolution in action because these dynamics are too slow in most organisms. To overcome this limitation, we sampled genomes from populations of Escherichia coli evolving in the laboratory for 10,000 generations. We analyzed the genomes for restriction fragment length polymorphisms (RFLP) using seven insertion sequences (IS) as probes; most polymorphisms detected by this approach reflect rearrangements (including transpositions) rather than point mutations. The evolving genomes became increasingly different from their ancestor over time. Moreover, tremendous diversity accumulated within each population, such that almost every individual had a different genetic fingerprint after 10,000 generations. As has been often suggested, but not previously shown by experiment, the rates of phenotypic and genomic change were discordant, both across replicate populations and over time within a population. Certain pivotal mutations were shared by all descendants in a population, and these are candidates for beneficial mutations, which are rare and difficult to find. More generally, these data show that the genome is highly dynamic even over a time scale that is, from an evolutionary perspective, very brief.

---

Of note, one author ont he paper, Richard Lenski, helped demonstrate that adaptive mutations do not evolve to adapt and organism to its environment but that random mutations are selected and as crashfrog pointed out, mutations occur in every generation i.e. you have mutations that niether of your parents carry i.e. new mutations.Elena SF, Cooper VS, Lenski RE. Related Articles, Links
Punctuated evolution caused by selection of rare beneficial mutations.
Science. 1996 Jun 21;272(5269):1802-4.Here is a summary of the error rates associated with DNA polymerase (it is much higher for other replication enzymes like reverse transcriptase)

quote:

---

Princess Takamatsu Symp. 1983;13:267-76. Related Articles, Links

​

Infidelity of DNA synthesis as a cause of mutagenesis.

​

Loeb LA, Liu PK, Das SK, Silber JR.

​

The concept underlying these studies is that a major determinant of mutagenesis involves perturbations in the fidelity of DNA replication. i.e., the accuracy by which DNA polymerases copy DNA templates. To investigate this relationship, we have designed in vitro assays to measure the accuracy of DNA replication and used these systems to screen for and to quantitate factors that promote errors in DNA synthesis. Using DNA polymerase from bacteria, the frequency of mistakes with phi X174 DNA as a template approaches 10(-7) and is similar to the spontaneous mutation rates in bacterial cells. In contrast, DNA polymerases from animal cells are more error-prone. The differences in fidelity among mammalian DNA polymerases which lack error-correcting mechanisms suggest that these enzymes enhance accuracy by improving base-selection. Thus, mutants in DNA polymerase-alpha might be altered in base-selection. Chinese hamster V79 cell mutants selected by resistance to aphidicolin, a specific inhibitor of DNA polymerase-alpha, have been reported (Somatic Cell Genet., 7: 235-253, 1981). DNA polymerase-alpha was purified from mitochondria-free crude extracts of these mutants by sequential column chromatography using DEAE-cellulose and phosphocellulose. DNA polymerase-alpha purified from one of the mutants is 10-fold more resistant to aphidicolin than the same enzyme purified from the parental cells. Moreover, the apparent Km for dCTP is 1.0 +/- 0.4 microM for the mutant polymerase and 10 +/- 4 microM for the parental enzyme. These observed differences are in accord with the known competition between aphidicolin and dCTP, and provide a mechanism for the aphidicolin resistance of the mutant, i.e., the decrease in Km for dCTP. The elevated spontaneous and induced mutation rate exhibited by this mutant could be mediated by the alteration in DNA polymerase-alpha. With DNA replicating enzymes from a variety of sources, enhancement of mutagenesis has been demonstrated by alteration in precursor pools, damage to DNA templates, loss of nucleotide bases on DNA, metal ions that interact with nucleotide bases, and organic compounds that intercalate into DNA. The alterations of deoxynucleoside triphosphate pools also occur after treatment of animal cells with known mutagens. This observation may provide a new mechanism for mutagenesis by these agents independent of alterations in DNA.

---

Finally, again related to cichlids, they speciate via hybídization in some cases and INCREASE their genetic diversity.

quote:

---

Mol Ecol. 2002 Mar;11(3):619-25. Related Articles, Links

​

Speciation via introgressive hybridization in East African cichlids?

​

Salzburger W, Baric S, Sturmbauer C.

​

Department of Zoology and Limnology, University of Innsbruck, Technikerstrasse 25, A-6020 Innsbruck, Austria.

​

Speciation caused by introgressive hybridization occurs frequently in plants but its importance remains controversial in animal evolution. Here we report a case of introgressive hybridization between two ancient and genetically distinct species of Lake Tanganyika cichlids that led to the formation of a new species. Neolamprologus marunguensis contains mtDNA haplotypes from both parental species varying on average by 12.4% in the first section of the control region and by 5.2% in a segment of the cytochrome b gene. All individuals have almost identical DNA sequences in the flanking regions of the single-copy nuclear DNA locus TmoM27, and show a mosaic of alleles derived from both parental lineages in six microsatellite loci. Hence, our finding displays another mode of speciation in cichlid fishes. The increase of genetic and phenotypic diversity due to hybridization may contribute to the uniquely rapid pace of speciation in cichlids.

---

So, to clarify some points from all of this, Faith is making both some overly general statements and some false statements.First, we know about random mutation not only from evolutionary studies but from analysis of the enyzmatic processes themselves i.e. the biochemistry of DNA and RNA polymerases. Anyone who works in a lab will get a spec sheet with the Taq polymerase they purchase indicating the measured error rate. In any case, as crashfrog indicated, we know from in vivo studies that even in humans, every individual carries novel mutations not present in their parents due to polymerase errors (I am leaving recombination and retrotransposition out at this point).We know that genetically isolated populations (or species) can form without a decrease in genetic diversity so Faith is overstating the case that it always leads to a reducition of genetic diversity. Selection might reduce variation at a single or several loci but this does not generally reduce all variation in a population or species. The reductions she is talking about are associated with strong bottlenecks or founder events which admittedly do occur but are not the only mechanism of isolation and differentiation of populations to form species.Finally, I have no idea where Faith gets the idea that separating populations causes suppressed genes or phenotypes to suddenly appear. All populations have variants that are distributed in different frequencies i.e. the blood groups or any other trait you want to measure. A founder event does not lead to the end of suppression of a phenotype/genotype...it merely means that if you have a 100 variants and 1 goes on to found a new population, that the frequency in the new population is a 1/100th subset of the variation of the original population..but that 1 individual was not suppressed in the original population.If you add selection into the mix, selection does not just decrease variation, it can increase it as well i.e.

quote:

---

Genetics. 2005 Aug;170(4):1897-911. Epub 2005 May 23. Related Articles, Links

​

High-diversity genes in the Arabidopsis genome.

​

Cork JM, Purugganan MD.

​

Department of Genetics, North Carolina State University, Raleigh, North Carolina 27695, USA.

​

High-diversity genes represent an important class of loci in organismal genomes. Since elevated levels of nucleotide variation are a key component of the molecular signature for balancing selection or local adaptation, high-diversity genes may represent loci whose alleles are selectively maintained as balanced polymorphisms. Comparison of 4300 random shotgun sequence fragments of the Arabidopsis thaliana Ler ecotype genome with the whole genomic sequence of the Col-0 ecotype identified 60 genes with putatively high levels of intraspecific variability. Eleven of these genes were sequenced in multiple A. thaliana accessions, 3 of which were found to display elevated levels of nucleotide polymorphism. These genes encode the myb-like transcription factor MYB103, a putative soluble starch synthase I, and a homeodomain-leucine zipper transcription factor. Analysis of these genes and 4-7 flanking genes in 14-20 A. thaliana ecotypes revealed that two of these loci show other characteristics of balanced polymorphisms, including broad peaks of nucleotide diversity spanning multiple linked genes and an excess of intermediate-frequency polymorphisms. Scanning genomes for high-diversity genomic regions may be useful in approaches to adaptive trait locus mapping for uncovering candidate balanced polymorphisms.

---

Coming back to my elephant example, Loxodonta cyclotis and Loxodonta africana are two different species. They can form hybrids yet introgression of alleles from one group to the other is very rare i.e. they remain distinct gene pools and have for over 1 million years. Jump up a level to the genus level, African elephants and Asian elephants are interfertile (one hybrid was produced)..however, the two genera are completely distinct genetically and have not formed a single gene pool for 5 million years. Elephants and manatees are more closely related genetically (and morphologically) than either are to any other species. They are even more reproductively isolated than among elephant groups....so what is the difference between the microevolutionary event (among elephant group differences i.e. savannah African elephants and desert elephants both in the same species) and the macroevolutionary event, manatee differences from elephantids other thant he time that separates them?

But its uniqueness does not exceed the genetic complement of the "species." And if it is a highly adapted (or genetically structured?) "species" (or breed/variety of the Kind) it most likely has a very limited gene pool. If a species/variety/breed is highly adapted to a particular niche, aren't we talking about a pretty hardwired genetic situation anyway? (what IS the term for the genetic situation of the cheetah -- I keep forgetting -- is it that it is homozygous? at some large number of gene loci, with NO alternate alleles -- I'm sorry if my language is klutzy, I have read about this stuff but the terminology isn't always accessible -- I picture it more easily than I label it) That is, you have this reduced genetic diversity situation I'm talking about in highly specialized "species" to a more noticeable degree.So yes, I get it that each offspring has a unique genetic makeup, but the more specialized the species it belongs to the less genetic diversity was available to choose from. So if we're talking about a cheetah cub, it is almost a clone of its parent, as there is just about zip genetic diversity. That is not so. What happened to Mendelian genetics if so? What does dominance and recessiveness mean if not something built into the population? It can't be something conferred willynilly by mutation. What does it mean to speak of numbers of alleles in a population? There are great numbers for some genes in some populations, small to even only one allele in others, and this has something to do with the built-in genetic picture as it gets worked on by the various Evolutionary Processes, not with random mutations. This whole process can be understood without reference to mutation at all, but only to normal built-in Mendelian genetics, to dominance and recessiveness and others I havenh't learned well enough, that is, to genetic potentials built into the genome that are reduced with each process of reproductive isolation. Mick did not mention mutation in his OP and did not mention it in answer to my discussion of the process either in his Message 29. Yes, and this is because of the greatly reduced genetic diversity which severely limits or absolutely prevents the emergence of adaptive traits. Again, the more specialization, the more "speciation" in other words, the less genetic diversity, the less adaptability, the less capacity to "evolve." I'm sorry I even tried to answer that question Mick asked phenotypically as it just created a useless rabbit trail. I am convinced that macroevolution cannot occur, meaning that there are indeed fixed "Kinds" that can only vary -- and vary quite widely in many cases to remarkable differences in phenotypic expression -- but are always GENETICALLY definable as that Kind and no other. I do not know how to define it but I am sure it will eventually be defined. I continue to believe that the "mechanism" that "prevents" macroevolution is the very processes called Evolutionary Processes we are discussing because with the majority of them (except for recombination and mutation) every new phenotype corresponds with a reduction in genetic diversity which is inconsistent with evolutionary requirements. If these processes are drastic or continue there is an absolute limit IN ALL DIRECTIONS of phenotypic change beyond which no further genetic change is possible -- without mutation of course. At that point recombination is usually not possible anyway. Mick is the only one who seems to be able to think about these processes in terms of ordinary genetics without the addition of mutation. It is puzzling to me that you and crashfrog talk as if mutation were the ONLY mechanism that confers diversity, as if you have no notion whatever of a built-in genetic complement which on its own accounts for the great majority of all phenotypic changes. How could mutation possibly be THE mechanism? Its randomness would prevent the predictable Mendelian combos and the coherent structures that appear in nature just for one point. A change in allele frequency in the population is produced by the Evolutionary Processes that I have been discussing throughout. All fecundity could possibly contribute is a speeded-up process of same. There is absolutely NO way to get a handle on this picture of random wild mutation as THE mechanism for all change in populations. Unique genotypes occur NATURALLY without mutations. They are produced by the selection of, say, recessive genes instead of dominant ones by migration or some other process. This exclusive mutation explanation is false on the face of it, as it denies the normal Mendelian ooperations, and something has to give here. What is Mick talking about in his Message 29 then, since he is not talking about mutations?This message has been edited by Faith, 11-28-2005 04:21 AM

I'm sorry, you are going to have to reduce your post to layman's language, and if possible reduce it to the briefest most schematic possible description, if you really care about my understanding it and being able to think about it.I believe I did acknowledge that there are situations which increase genetic diversity, but that the preponderance of the reduction of genetic diversity through the usual Evolutionary Processes seems hardly to be met let alone counteracted by such situations.This message has been edited by Faith, 11-28-2005 04:32 AM

quote:

---

That is not so. What happened to Mendelian genetics if so? What does dominance and recessiveness mean if not something built into the population? It can't be something conferred willynilly by mutation. What does it mean to speak of numbers of alleles in a population? There are great numbers for some genes in some populations, small to even only one allele in others, and this has something to do with the built-in genetic picture as it gets worked on by the various Evolutionary Processes, not with random mutations.

---

Faith, you have some deep misunderstandings about genetics and mutation. Mendelian genetics is the study of the segregation of mutations by hereditary transmission from one generation to another! Dominant and recessive is the phenotypic expression of a genetic mutation such that if one mutation is Dominant, the phenotype it confers will be expressed whether in the presence of the recessive mutation or in the presence of another identical sequence. Dominant and recessive traits are determined by mutations! Genetics has everything to do with mutation. Mendel only looked at traits that affected phenotype because at the time the basis of heredity was unknown.What does it mean to talk about number of alleles in populations? Simple, you have two copies of every nuclear gene in your diploid genome. If to copies of one gene differ by a point mutation, you have two alleles. The genes can differ in many different places. Each difference is an allele. For some genes, there are hundreds of different versions of the same gene in the population occurring at different frequencies. Population genetics and evolution measure how these frequencies change in response to selection, isolation, etc.You, me, crashfrog, all of us are "mutants" we carry errors that occurred as our parents DNA was being replicated during meiosis.There is no built in anything genetic except that DNA polymerases are very error prone and thus, every individual generates novel alleles in each generation. There is not built in variation...it increases and decreases depending on which is stronger, the selection against specific variations or the tolerance of a lot of errors. This can be measured in a test tube, in captive populations and in the wild...and even in human patient samples.

quote:

---

This whole process can be understood without reference to mutation at all, but only to normal built-in Mendelian genetics, to dominance and recessiveness and others I havenh't learned well enough, that is, to genetic potentials

---

Genetic potentials so not exist..and as explained, mendelian genetics is all about mutation..mick did not reference mutation because he assumed everyone knows that the variation he is talking about represents mutation events...there are no genetic variants without mutation..they are the same thing...this is Genetics 101.

quote:

---

Yes, and this is because of the greatly reduced genetic diversity which severely limits or absolutely prevents the emergence of adaptive traits. Again, the more specialization, the more "speciation" in other words, the less genetic diversity, the less adaptability, the less capacity to "evolve."

---

Except that every study from cichlids, to mice, to flies, to bacteria demonstrates exactly the opposite of what you state here. Richard Lenski has even demonstrated that specific mutations are selected for under experimental conditions which is followed by an explosion of genetic diversity within a mere 10,000 generations.

quote:

---

I am convinced that macroevolution cannot occur, meaning that there are indeed fixed "Kinds" that can only vary --

---

Not to be mean but considering you clearly do not have a background in any of the relevant biology, being "convinced" that something cannot occur is extremely premature and frankly insulting to those of us well versed in the subject...to put it in a way that you might understand, for sake of argument say I never read the bible. what if I told you that I am convinced that there is no mention of Jesus in the New Testament? I don't know anything about the Bible but I am still convinced my belief is correct. You would not find this arguement compelling would you? Well, you are making exactly this arguement with respect to macroevolution.

quote:

---

Mick is the only one who seems to be able to think about these processes in terms of ordinary genetics without the addition of mutation

---

Every variant in mick's paper, every allele, is a mutation....ORDINARY genetics is the study of how genes mutate and spread from one individual to another.

quote:

---

Unique genotypes occur NATURALLY without mutations.

---

Please show how...this would falsify Mendelian genetics if it could be shown and the several hundred thousand published studies on genetics and genomics have failed to demonstrate such an effect...Here are some websites to help you out.One on Mendelian geneticshttp://www.ndsu.nodak.edu/...lean/plsc431/mendel/mendel1.htmhere is another, pay attention to how mutations and alleles are definedhttp://www.athro.com/evo/gen/genetic.htmlhere is wikipedia
Allele - WikipediaNote, the only way to get an alternate DNA sequences is via mutation..thus all alleles are mutants whether they confer a negative or positive or neutral result on the phenotype of the organism.

Ok,
that mutations occur randomly and frequently is a measured biochemical property of all polymerases i.e. the enzymes that replicate DNA. That is one issue.Alleles are the result of this error prone replication mechanism, again measurable in the lab and in the wild.Selection can reduce the number of alleles in a population..but it can also increase it as in the case of cichlids and in bacteria. Evoltion is the change of allele frequencies over time within species, between species, and among higher taxanomic groups..whether macro or micro..the same process is at work.In any event, once two populations have become reproductively isolated, they continue to generate new variants with each offspring...we are all mutants for some locus or another. that is the point of Lenski's work on bacteria. It is also the point of the work on cichlids.the "usual Evolutionary Processes" means nothing to me. Care to elaborate?

I was referring to genetic recombination, including "crossing over" of chromosomes, which occurs through meiosis in sexual reproduction, or through conjugation and transduction in bacteria.You've made a lot of positive assertions in this thread, and I think it's time that you backed them up, especially since you're now at the point of telling people that they "don't get it."

So, you don't know.Let me tell you. Individuals possess both "genotype" and "phenotype"; genotype is their specific set of genetic characteristics, and phenotype is their specific set of physical characteristics. Whether they have green eyes or blue. Whether they're tall or short. Those things constitute an individual's phenotype.Phenotypes vary between individuals because individuals have varying genetics (genotypes.) Absolutely none of those processes will result in phenotypic variation. Rather, those processes contract and reduce phenotypic variation by contracting genetic diversity. Phenotype is the physical expression of genes. Any contraction in genetic diversity must result in a contraction of phenotypic diversity.Genetic diversity expands as a result of mutation. Also, sexual recombination is a source of additional phenotypic variation, but the effect is more relevant to selection than to mutation. We're having a problem because you're using the word "phenotype" without actually knowing what it means.

Explain why. Explain, surely a human is highly adapted? Perhaps you mean 'specialized'? What difference do you think this makes? Hardwired? They obviously have a range of genes that will allow them to survive in that niche, but that range of genes depends where in that niche they are, and its a massive range in the vast majority of situations anyway. If said organism is capable of surviving in another, similar (yet different) niche, then they might migrate as population size increases so much that it makes sense to do so. I believe you have it about right, also one could say 'monomorphic'. Here is an interesting study about it. I don't think this is of import to this conversation though, it doesn't seem to be anything to do with the cheetah being highly 'specialized', and even if it was, that just means nature abhors over specialization (which she does since changing times will lead to extinction, meaning the cheetah may well be an evolutionary dead end). So yeah, bottlenecks can cause serious problems for populations, especially ones to the magnitude that the cheetahs are hypothesized to have gone through (I've seen one hypothesis that goes as far as proposing only one surviving pregnant female after their near extinction event...many genes were lost...there's a nice 'pop' article on it here.A more technical look at bottlenecks can be found hereI'm not sure if that's the case. Do you have any other examples of highly specialized organisms with this problem? Mendelian genetics is just the genetics of heredity. Without mutations, we'll just find that either the most dominant gene fixes into the population so that all members have it, or, if the dominant gene is selected against, it will vanish from the population. No novel features would arise, and the organisms will at best enter into an evolutionary stasis or will die off. It does mean that very thing. The genes that are already built into the population. It is difficult to see how even a decent amount of microevolution is going to get underway with just Mendellian genetics to go off. I don't understand. A mutation occurs which forms something novel. The gene involved may or not be dominant depending on its makeup. I don't think 'willynilly' is proposed to be involved at any stage. Right, but wrong. The alleles frequency is 'built in' by mutations and natural selection. The 'gets worked on by the various Evolutionary Processes' happens by basically selecting out those alleles that do not survive to mating.One organism has a random mutation that increases the thickness of its fur. It does not convey a disadvantage in this case and so the mutation gets distributed throughout the population. If 20% of a population has the 'thick fur' gene, then we would see it 1 in 5 chromosomes (this is the allele's frequency). If the environment was to get colder the thick fur gene may well increase the survival chances of those with the gene, so the frequency might change to 50%. Thus: mutations cause alelle changes, selection decides which allele changes stick around, and which ones get weeded out. It can't be understood without reference to mutation. Without mutation, very little happens! If you don't reference mutation, you can't understand the whole process. He mentioned it in the OP, but it wasn't the focus of his discussion since he was talking about the structure alelle differences in populations and their relations to geography, and how at small levels the same processes are at work as they are at bigger (more macro) levels. He wasn't really discussing the mechanism for those alelles getting there. That is one cause for extinction yes. I'm not sure this is the case. Maybe it is with regards to specilalization, but I don't see how more speciation leads to less genetic diversity. Speciation and specialisation aren't equivalent. And specialization doesn't imply low genetic diversity (that would need a major bottleneck) Its surely the case that a highly specialized organism is more fragile, but I don't see the case that a very light selective pressure can't change the course of a specialized but suitably diverse population. That's fine. That's OK too. The problem comes when the claim is made that macroevolution cannot happen, with no definition of macroevolution. How can one make an absolute statement with non absolute terms? Your statement is fine, its clearly worded as opinion. OK. I don't think one can look at the number of processes that 'select' versus the number of processes that introduce novel features (including epigenetics and mutation) and draw any sort of valid conclusion. I think the impact that each of these things have should be weighed.Do you have any evidence that every new phenotype corresponds with a reduction in genetic diversity? It would be inconsistent with evolutionary requirements so it would be interesting to see this. Because Mick isn't talking about how alelle frequency changes, he's just talking about the alelle distribution. Its only when you start bringing up objections of around new genetic information, bottlenecks, and so and start discussing the mechanism for alelle frequency change that we need to include mutations.If you look at the OP, however, Mick clearly writes:

quote:

---

We can base our understanding of this data on the microevolutionary principles that Tamias amoenus arise from a single common ancestor and that the descendants of that ancestor have spread across the range, accumulating mutations along the way which have been preserved in each geographical region by heredity

---

Indeed, his entire point seems to be that the same process that results in microevolution (variations within a species, and from one species to another), seems to follow the same pattern as those observed at higher levels of evolution (approaching macroevolution? variations between genus), a genus would be something like Feline, Panther and Lynx, which I suppose isn't true macroevolution just yet, since after all, they are all still 'cats'. This is the reason I'm not sure of Mick's conclusion at this point. If he can expand to include higher (or perhaps it should be lower) taxonomic levels, I'd be more impressed. Well, no, there are other factors, such as epigenetics as I previously mentioned. Hmmm, maybe Faith, but you brought mutation up, I was just pulling you up on not including mutation's important brother, selection, which has led us to this point. Unless some kind of selection process was involved, sorting the 'bad' from the 'good' so that the 'worst' don't survive, and the 'better' ones mate more (thus increasing their frequency). Mutation and natural selection being the most famous evolutionary process to change the frequency of alleles. Let us take an adult population whose size remains constant at 10,000 members. Each female has 24 offspring (2 litters of twelve for two parents) per generation so we end up with 10,000 adults and 120,000 children. Eventually the old adults die, and the children take up the mantle. However, the niche can only handle 10,000 adults so 110,000 children have to die. Only 9% of the kids get to mating age. There is tremendous struggle to survive going on here, and only those that are best at it manage. Given that all of the kids had a unique genome, and given that each one was a unique genetic mutant, only the genomes that convey an advantage survive, therefore the advantageous alelles brought about by mutation fix in the population, and the disadvantageous ones get weeded out.Without fecundity the struggle to survive is massively limited, so deletrious mutations are more likely to acrue and fix. Fortunately fecundity exists and is an essential aspect of evolution as picked up even by Darwin. It isn't THE change, that's why. First comes the mutation, then comes the selection. Other factors are at play, gene transfer, epigenetics and so on and so forth. Well quite, but I don't think a population which had no mutations would last long unless it started with high genetic variety. I don't think it would ever speciate (ie become sexually incompatable with its ancestral population) either. Not a whole lot would happen at all really. And of course, this screws asexually reproducing organisms royally....every one (well a great deal anyway) would be a perfect clone of its ancestor. Well that's not true. Mendelian operations tell us about heridity, and functions perfectly with the mutation explanation, which as I have said in this post and in others is not proposed to be an exclusive explanation, indeed, it cannot be an exclusive explanation, but neither can it be ignored when discussing population genetics. Looks like he is talking about phylogeography and the well established and accepted evolutionary processes. He doesn't specify what those established evolutionary processes are, since he doesn't go into detail about the nature of these processes he is unlikely to discuss mutations, epigenetics, gene transfer, selection etc is he?Tell me, what was mick talking about in Message 1 when he said: This message has been edited by Modulous, Mon, 28-November-2005 03:50 PM to fix a maths errorThis message has been edited by Modulous, Mon, 28-November-2005 04:48 PM