Summations Only

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A key problem in evolutionary biology is to connect genotype with phenotype for fitness-related traits.

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It is apparent that the conclusion in your citation for changes in color of the studied mice (second paper) are the result of expressions of different alleles in the genome (a start codon disruption).

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The black-and-tan mutation in the laboratory mouse produces a dark dorsum with unbanded hairs and is caused by an insertion disrupting the dorsal promoter, ≈15 kb 5′ of the start codon (15). We reasoned that a similar mutation in C. intermedius might be detected through linkage to polymorphisms at neutral sites over moderate genomic distances (0—50 kb, depending on the age of the mutation). We observed 16 single-nucleotide polymorphisms and 5 insertion/deletion polymorphisms, including several at intermediate frequencies; none showed an association with coat color.

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Reference (15)

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We demonstrate that the distinct insertions in a, a(t) and Aw cause pigmentation differences by selectively inactivating the expression of different forms of agouti transcripts.

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The genetic basis of adaptive melanism in pocket mice - PMC

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Creationists never disputed any particular advantage of random insertions in gene sequences used for adaptation; but only if regulated by genomic programming. This principle is obvious in the immune defense mechanism of higher mammals to anticipate infections as well as changing the expression of preexisting gene sequences; for mice color and other phenotype characteristics. Creationists have always maintained that random mutation with out regulation is disadvantageous or antithesis to an organism. In other words, the mutations are to provide adaptation of the genome. It is contrary to the evidence that these types of mutations are capable of a speciation event in an organism. This rules out mutations as a mechanism for evolution but promotes the viewpoint of mutations for adaptation. Edited by zaius137, : No reason given.

(jar) my friendWebbed feet in a dog probably would not be from genetic drift. More than likely such an occurrence would be from a detrimental mutation in a single individual. You have not made any suggestion on how such a mutation could be fixed in a population since breeding with a normal dog would probably mask the deformity (dogs are diploids). Anyway, a dog is still a dog not another species; albeit deformed.

Good to talk with you Wounded King Sorry, about my confusion about who cited these articles. Frankly, these articles are an exercise in disrupting preexisting gene sequence to illicit the relative functions involved. What are these citations intended to prove about new unique functionality? Clearly, these alleles preexist in the genome and are not receiving new novel coding sequences (long additional strings of base pair coding) but only experiencing shifts in ORF’s.

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Mutations at both agouti (14, 15) and at Mc1r (16) have been identified that produce unbanded dorsal hairs in the laboratory mouse. We observed banded dorsal hairs in all light C. intermedius, but unbanded, uniformly melanic hairs in all dark C. intermedius, suggesting a possible role for either agouti or Mc1r.
We used association studies with these candidate genes to investigate the genetic basis of adaptive melanism in C. intermedius. Here, we report that mutations at Mc1r are perfectly associated with coat color differences in one population of these mice, but that another population of mice shows no association between Mc1r mutations and coat color phenotype.

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The genetic basis of adaptive melanism in pocket mice - PMC

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What known mutational mechanisms are you referring to would cause an allele arising with only 3 or 4-point mutations? I would say that this is only modification of existing alleles. What would you say this is? How is this argument contrary to the concept of preprogrammed alleles? I would say that there is a lack of understanding of the entire process by the authors. I could easily say that the unknown correlation between specific alleles show a fluidity in the genetic structure. Is this fluidity designed or not that is the underlying question here? Actually DNA ORF’s frame shifting. Yes but the ORF is shifted away from that start codon (the expression is changed). Please explain what is so complicated about this to understand? Maybe I can best express my perspective from a personal viewpoint.I have used random number generators in programs to produce unique program behavior. In other words, my program used the advantage of a random variable to produce useful output. If somehow the random variable was inserted in my core program, the result might crash my efforts (if the exception was not handled properly). Yes the immune system is adaptive in this exact way. Thanks for the exercise in explaining the very processes I am pointing out. If you do not like anticipation, try preemptive or fluid. It is an amazing irreducible system. I am not sure if we can sidetrack on this issue (it has been covered by intelligent design posts). The mechanism is easy to research and is covered by Michael J. Behe. Please provide an example of an observed spontaneous molecular mechanism for the occurrence of a single gene outside the mechanism of duplication. Contrary to the observed evidence, my friend. Drosophila melanogaster is probably the most observed and scrutinized organism in science. For over 80 years scientists have tried all forms of mutagens, cross breeding, inbreeding and there has never been an observed speciation event in DM. The article you cited uses several standard analysis tools geared for inferring common descent and evolution; sorry but this is evaluative speculation at best. The following excerpt from the article lays out my objection:

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However, almost nothing is known about the genes involved in such hybrid incompatibilities or the evolutionary forces that drive their divergence. Here we identify a gene that causes epistatic inviability in hybrids between two fruitfly species, Drosophila melanogaster and D. simulans. Our population genetic analysis reveals that this genewhich encodes a nuclear pore proteinevolved by positive natural selection in both species’ lineages. These results show that a lethal hybrid incompatibility has evolved as a by-product of adaptive protein evolution.

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Here is an article summarizing some of the efforts to cause DM to evolve:

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After decades of study, without immediately killing or sterilizing them, 400 different mutational features have been identified in fruit flies. But none of these changes the fruit fly to a different species.

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2021, 10 Damage to the genome can and does cause reproductive problems but not speciation events. Separated species can be forced to breed and thus show that reproduction in the same species is maintained. Macro changes in genotype are not observed even in separated and reproductive isolated organisms. I would like some examples of yours for my notes. My example is Drosophila melanogaster.I appreciate your knowledge about the subject. Let us reason further on this subject.
Thanks for the citations WK Edited by zaius137, : No reason given.

Wounded King my friend Your statement implies that these existing alleles just magically appeared in the first place. They are in the right place at the right time to accept moderate modifications to create novel functionality. I have seen no evidence from you or anyone else demonstrating any new novel phylogenic functions arising in the genome except by genetic recombination. Actually, my statement is derived from the fact these phylogenic characteristics for coloration has escaped the scope of these researchers hypothesis and they jump to the speculative conclusion that:

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indicating that adaptive dark color has evolved independently in this species through changes at different genes.

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Simple balderdash A presumptuous conclusion since they did not specifically identify the genes or process. This particular paper does not make any real findings about multiple alleles in different groups of the same species being responsible for different coat coloration. They just make speculation to explain why there approach failed. Yes, I did read the paper I think your point of novel functionality is better served if there actually were a frame shift by promoter disruption. The alternative is saying damaging genes promotes new and unique functions. Removing components to improve working devices is not uncommon though (but the device is always degraded). I recall a certain self-taught engineer in the 60’s used a similar approach to evolution when engineering electronic devicesConsider the following Earl Madman Muntz

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In the 1940s and 1950s, televisions were very complex pieces of equipment, often containing upwards of 30 vacuum tubes, as well as transformers, rheostats, and other heavy electronics. The consequent high price limited their potential for high volume sales. Muntz determined, through trial and error, that he could remove a significant number of parts and still end up with a monochrome TV that worked very well in urban areas, close to transmission towers. He literally carried a pair of wire clippers around and when he felt that one of his builders was overengineering a circuit, he would begin snipping components out. When the TV stopped functioning, they would reinsert the last part and leave the TV as-is. As a result of removing tubes and greatly simplifying circuits originally designed to boost function in fringe areas (far from transmission towers), Muntz's sets generated less heat; overheating was one of the most common reasons for failure in early sets. The sets also weighed significantly less, because as the circuitry was reduced, smaller in-set power supplies were needed. Additionally, as the power supplies contained expensive copper this further reduced cost.
Madman Muntz - Wikipedia

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Interesting that FGF4 retrogene was found in the wolf; this seems to indicate that the chondrodysplastic phenotype in dogs is just another characteristic that follows Mendelian genetics and it might be correctly said it is a pre-existing characteristic in dogs.

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To further understand the origin of the fgf4 retrogene, we compared haplotypes from the source gene, the retrogene, and the insertion site in both dogs and their wild progenitor, the gray wolf. An Expressed Fgf4 Retrogene Is Associated with Breed-Defining Chondrodysplasia in Domestic Dogs - PMC

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However, since we find a common haplotype of 24Kb surrounding the fgf4 retrogene in 19 short legged breeds it is likely the chondrodysplastic phenotype arose only once, before the division of early dogs into modern breeds. Thereafter, the retrogene and its associated phenotype were both maintained and propagated by breeders for purposes specific to each breed. An Expressed Fgf4 Retrogene Is Associated with Breed-Defining Chondrodysplasia in Domestic Dogs - PMC

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Therefore, what is the point here? You know I am going to claim pre-existing programmed gene sequences and all the evolution nonsense is just that nonsense. How does Ecological genetics actually work on the molecular level maybe I am talking to a future Nobel Prize winner? Please don’t get your panties in a wad the answer is yes by the way. It identified one polymorphic aspect between two separate species, fine. However, conclusions about there common descent is just speculation. This from a related article...

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These results show that a lethal hybrid incompatibility has evolved as a by-product of adaptive protein evolution. Adaptive protein evolution in Drosophila - PubMed

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You are now making presumptuous statements.

My friend Wounded King You can end your accentus objection; at this point, I am only using the phrase as a foil. And those man instances are? And back via AD Nauseum to that paper that you want to continually use to torment me From citation (15) in that paper Do I see inactivating here? They don’t mean inhibiting existing expression to alter pigmentation do they? But these changes in pigmentation are not really creating new novel traits right. Do really wish to make a straw man out of this? I am amazed on how obtuse someone can get and how it can slow down a conversation. The FGF4 haplotype and insertion site is in the grey wolf. It is one mutation away (a single retrotransposition event). Therefore, you have another example of an existing allele slightly modified to shorten legs of an organism (this also is a degradation of an existing allelic expression).Now you need to get on with the show and demonstrate how unique and novel features arise from any other way but simple modifications to complex alleles and if these modifications are unique and novel. You are correct they did not find the actual retrogene inserted it the wolf but all the necessary genetic code is present. This does not sound unreasonable because if the retrogene appeared in a wild wolf that wolf might not be alive long enough to enjoy benefits of short legs. Unbiased scientific research always bolsters my position. If that were not true, I would not say it. Unfortunately I usually must wade threw evolutionary nonsense and biological machination to get to the point. Does that mean we are no longer friends? I find that every conversation I have it is always beneficial to show some respect to the other individual. I have always found some unexpected opportunity to learn something new from everyone. If they are the same species fine, remember common descent of one species to another is your position not mine. There are different species of fruit flies you know and I do not believe they all came from one ancestor. None of your arguments really seems to want to answer any of the real dilemmas in the new evolution synthesis. Namely:How the modern evolution synthesis can account for

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evolution in terms of changes in gene and genotype frequencies within populations and the processes that convert the variation with populations into more or less permanent variation between species.

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You know the old microevolution, macroevolution thing.
Mostly your examples are reversible when it comes to allele mixing.
Let us get to where and how these new novel innovations or microevolution changes fix in a population
Or is this pushing the thread outside the limits of discussion a convenient escape for the harder questions.Edited by zaius137, : No reason given.

Tangle my friend.. Creationists have always maintained the need for adaptation but the adaptation is not fixed permanently and irreversibly into the genome of a population (speciation). Creationists also believe that there are specific areas in genome that can accept this variation without fatal effects to the genome. We cannot deny that since the fall of mankind in the garden such deleterious mutations happen all the time but as you know humans are diploid and can absorb a heavy loading of the genome. These deleterious mutations may continue to propagate in a particular race of individuals and are not necessarily reversible when outside the adaptive mechanism of the genome (they persist because of the curse of the fall).The burden of the Evolutionists have been to explain the connection between genotype and phenotype by a number of proposed mechanisms. One important principle is called classic sweeps which hopes that variations eliminate heterozygosity so that the change in phenotype is made permanent in the genome and irreversible in a breeding population (fixed permanently).About fruit flies:Empirical evidence has shown Darwinian evolution is inadequate in bolstering evolution by natural selection. Consider the following examining Classic Sweeps in fixation of traits in a population.

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"Recent research on evolutionary genetics has focused on classic selective sweeps, which are evolutionary processes involving the fixation of newly arising beneficial mutations. In a recombining region, a selected sweep is expected to reduce heterozygosity at SNPs flanking the selected site. [. . .] Notably, we observe no location in the genome where heterozygosity is reduced to anywhere near zero, and this lack of evidence for a classic sweep is a feature of the data regardless of window size."

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http://www.arn.org/.../experimental_evolution_in_fruit_fliesIn other words the old alleles remain present in subsequent generations and are not swept clean from subsequent generations. Stasis in a species is the observable evidence. Species of fruit flies have always been a species of fruit flies.Fixation in the genome must be discussed when talking about New and Unique traits appearing by evolution.

Tangle my friend, Maybe it is my problem in not being specific about my statementsTalking specifically about the mouse paper I do commit to the following statements. I hope you are not expecting a yes or no about this. There were findings in the paper but I purpose the conclusions to be all wrong.I do not believe that the authors of this mouse paper correctly identified all the genes and types of mutations involved or even a connection between the color adaptation and a molecular mechanism for the selection pressure of coat coloration.Without doubt, some mutations add beneficial adaptations to the genome when they occur in the proper positions (I think everyone here can agree on that). The big question is exactly how many mutations are necessary and how many genes are involved to create these adaptations; new discoveries are now breaking news in genetics (the fruit fly citation).Evolution of a Fruit Fly, Evolution of a Human | GenomewebIt is clear in your cited mouse paper that the authors are making assumptions that a single mutation to a single gene is changing coat color. The authors made further speculation that a different mutation in another gene in a separate group of mice was responsible for similar coloration change in that group. However, they drew their conclusions without identifying that particular gene or type mutation. In my opinion, this mouse paper, on that basis, is total nonsense.If new studies with fruit flies is correct this single point mutation paradigm in a single gene to cause a change or the proposed permanent change is completely wrong (see soft sweeps in genetics). There is observed evidence that there are far more complicated connections between genes and mutations than evolutionists currently understand. Evolution in fruit flies is inhibited by these new findings, which only demonstrates the claims made by creationists all along.

Tangle my friend. Unfortunately, you mix up what comes first in selective pressure. You see there must be certain coloration of mice first before there is any kind of selection to take place. Therefore, if you talk about sexual selection then the mutation or alleles are already expressed in the population and all the predators have to do is select those individuals that do not express the beneficial coloration (Concentration of specific alleles).
You see mouse coloration is pre —existing so you cannot say it has arisen because of natural selection. Remember, survival of the fittest is not creation of the fittest.Let’s see some ware in this thread one of has claimed that the genetic structure was pre-existing. Who was that?Now you have a population of selected individuals with concentrations of beneficial alleles for camouflage. Was the development of beneficial coloration a new and novel trait? No because it had to show up before selection could even work on it. Is other populations of this species devoid of these alleles? No again, because other members occasionally show up with the desired coat color under lower selective pressure (or neutral pressure) because of Mendelian genetics.Again the crux of your argument must consider fixation of these mutations in a population before you can actually say these Novel Traits arose and are not just deformed individuals.By the way, when I refer to molecular mechanisms it is not sexual reproduction.

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Environmental stresses and stimuli cannot exercise the creative causation of highly complex pre-coded genetic information that underlies irreducibly complex systems of adaptation.

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Mechanisms of Adaptation in Biology: Molecular Cell Biology | The Institute for Creation Research
Keep the thought process going there is always room for one more creationist around here.

Tangle my friend... I have a question; does every color change await a mutation of a gene? There must be an underlining adaptable mechanism built into the genome. If natural selection is the main mechanism of causation, there has to be a molecular interface between the resulting gene and environmental pressure. This interface should be discernable and explainable.Why is there heterozygosity of coloration remaining in the selected population of mice if say black mice are selected to be more fit?

Tangle my friend.
Oh boy another mouse paper. Thanks for your citation; was this linked in the last paper? . Ecological genetics of adaptive color polymorphism in pocket mice: geographic variation in selected and neutral genes - PubMedTwo thumbs up for Natural Selection and microevolution.

jar my friendAgainTwo thumbs up for Natural Selection and microevolution. Tan and Dark gray mice remain reversible. However, the pink with yellow and green stripes seem to be engineered by Man (expression of latent maniacal humor). So now exchange the two populations to the others environment. I bet that the tan mice turn dark grey and the gray mice turn tan. Microevolution is reversible.

RAZD my friend You are actually saying that mutation alone is generating mice coloration; then it is somehow fixed in a population to be recalled later by natural selection.First you must deal with the consequences of fixation in a population (see Haldane). Then you must preserve these changes against sweeps of phenotypic variation but be able to expose these changes to the organism under selective pressure. This says nothing about the origination of these genes in the first place.The process you describe above seems very simple on the surface and very Darwinian. The only problem is that such propositions are highly problematical and have not yet been described by the evolutionist in terms of molecular mechanisms.

RAZD my friendYour scenario is right in line with most evolutionists’ beliefs (that is the good news) but those suppositions do not hold up under scientific investigation (that is the bad news). The problem is it has never been observedDo you know who Haldane is? Major evolution calculations are based on Haldane’s work.

Dr. Adequate my friendDo you know who Haldane is?

Wounded King my friendI honestly enjoy your understanding of genetics (it is far better than mine is). I completely follow your explanation here (thanks) but the further connection between the mutations in Mc1r giving rise to a more sensitive receptor balance seems to me as a vague connection (although cited in the paper). What do these mutations actually accomplish in the mechanism for coloration changes; are they the sole control of the balance of cyclic-AMP and do these various papers make that proper connection? So is the loss or gain-of-function in the melanic pocket mouse still a case of allele mixing or is it because of mutations on Mc1r (a polymorphism in that species)? Overall, I am leaning to the former. I maintain that coloration in this mouse is reversible in all populations. If indeed these mutations are the mechanism for tipping the balance of (cAMP) then genetic recombination reverses the process (by gene flow). Very interesting but if anything, this only points to a very fluid adaptation mechanism (very Mendelian and not unique new traits as some participants would suggest). The dilemma you pose might be rectified to a certain degree by examining other genomes, maybe those of a fruit fly or E. Coli. Regulated populations of fruit flies combined with long-term studies provide a better-defined ancestral population. Here is some interesting finding in fruit flies indicating a very complex interaction between genes (not just one or two as the paradigm exists) and a overall tendency to retain Heterozygosity.http://www.arn.org/.../experimental_evolution_in_fruit_fliesI suggest that the adaptive mechanism is the sole novel new trait source. The mechanism in question defies the Darwinian explanation via gradualism. It is a mechanism that cannot arise by processes of chance and it transcends the idea of point mutations in its origin; it is like asserting that a machine can produce itself before there were any other machines present. It is God created.