Evolution extinction Intelligent Design Natural selection

Can sexual selection cause a decline in evolutionary fitness?

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From evolutionary biologist Richard O. Prum at the New York Times:

Are These Birds Too Sexy to Survive? Natural selection can’t explain this.

Wow. Careers have been wrecked over such departures from dogma.

Most biologists believe that these mechanisms always work in concert — that sex appeal is the sign of an objectively better mate, one with better genes or in better condition. But the wing songs of the club-winged manakin provide new insights that contradict this conventional wisdom. Instead of ensuring that organisms are on an inexorable path to self-improvement, mate choice can drive a species into what I call maladaptive decadence — a decline in survival and fecundity of the entire species. It may even lead to extinction.

But wait! Don’t most of us know guys like that? Ask around at half-way houses.

Evolved decadence may turn out to be common. For instance, the male Wilson’s bird of paradise has a bright blue, bald crown — a disadvantage when hiding from predators, but handy when it comes to courting a female. The females have the same risky tonsure, albeit in a deeper violet hue. The male wire-tailed manakin has elongated tail feathers, which he swipes across the face of the female during courtship, and which may impede flight. Once again, the females sport the same long feathers. Even the peafowl has a longer tail than she needs.More.

Even we didn’t realize that Darwinism was that rigid in its thinking. Again, wow. 😉

See also: Can sex explain evolution?

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46 Replies to “Can sexual selection cause a decline in evolutionary fitness?

  1. 1
    hammaspeikko says:

    Wow. Careers have been wrecked over such departures from dogma.

    Scientists who agree with evolution say this all the time without it hurting their career. Larry Moran is an example. His career may be winding down, but that is due to his age, not his opinions on evolution.

    With respect to sexual selection decreasing fitness, I don’t see how that is possible. Sexual selection is a form of natural selection that is caused by differential mate selection. If it is decreasing fitness then it isn’t selection. Fitness is measured relative to the entire population. Even if mate selection results in lower fecundity from one generation to the next, this could still be an increase in fitness if the trait selected for still has a higher fecundity than those without that trait.

    However, it is quite possible that selection, sexual or otherwise, can lead to an evolutionary dead end. This is fully consistent with evolutionary theory.

  2. 2
    anthropic says:

    Yes. Sexual selection increases fitness. Unless, of course, it leads to an evolutionary dead end. Either way, evolution explains it, just as it explains everything that happens.

    Uh-huh.

  3. 3
    hammaspeikko says:

    Anthropic, fitness and long term survival are not the same thing. Fitness of a phenotype can increase over a couple generations even if the reproductive rate dramatically decreases. For fitness of a specific phenotype to increase, all that must occur is for the reproductive rate of those with this phenotype to increase relative to those without this phenotype.

    For example, let’s assume there are two phenotype in a population.

    1) an environmental change results in a significant reduction in reproduction rates for both phenotypes
    2) phenotype A experiences a 50% decrease in reproduction.
    2) phenotype B experiences a 75% decrease in reproduction.

    Because fitness is measured relative to the rest of the population, phenotype A has increased in fitness even though it has seen a dramatic reduction in reproductive rate. This is evolution 101 stuff. And, as you can imagine, continuing along this course could result in the extinction of the population.

    That is why I said that selection does not reduce fitness. It can only increase it. Otherwise, by definition, it is not selection. But selection also does not guarantee survival. If selection pressures are very high over a short period of time, the natural genetic variation that has built up in a population over time will be significantly reduced. Any further pressures could result in the population not surviving. Evolution 101 again.

    There are many things that evolution doesn’t explain. But this isn’t one of them.

  4. 4
    LocalMinimum says:

    hammaspeikko:

    So, fitness excludes any notion of sufficient functionality/survivability? What an incredible misnomer Darwin wielded. I suppose you can easily become fit for extinction.

  5. 5
    asauber says:

    hammaspeikko,

    If it is decreasing fitness then it isn’t selection.

    What impels natural forces to “select” increasing fitness over decreasing fitness?

    Andrew

  6. 6
    LocalMinimum says:

    To answer myself I suppose the argument would be: “anything below minimum functionality will automatically be selected against”, so I guess the issue would be more along the lines of “non-local” or minimum general functionality, i.e. how quickly does a genotype become critically incapable of maintaining population size against probable/inevitable fluctuations in selection parameters. A little more nuanced.

  7. 7
    asauber says:

    It almost sounds like natural selection (whatever animates it) has a preference for Life.

    Andrew

  8. 8
    PaV says:

    hammaspeiko:

    That is why I said that selection does not reduce fitness. It can only increase it. Otherwise, by definition, it is not selection.

    IOW, evolution is the survival of the fittest. And therefore, by definition, those who survive are the fittest. And how do we know they’re the fittest? They survived!!

    This is circular logic, typical of evolutionists.

    Here’s what I mean. I’ll use your example of Phenotypes A and B.

    You wrote:
    For example, let’s assume there are two phenotype in a population.

    1) an environmental change results in a significant reduction in reproduction rates for both phenotypes
    2) phenotype A experiences a 50% decrease in reproduction.
    2) phenotype B experiences a 75% decrease in reproduction.

    Okay. So, let’s say there was a disease that affected certain trees in the area, and this disease was found only in its uppermost parts.

    Now, phenotype A is a bird species with smaller wings, and less adapted to flight. So, it spends more of its time feeding on the ground, and less in the trees, especially in the top most portions of the tree.

    Now, phenotype B is the same species, but with slightly larger wings, and better adapted to flight. It feeds on the tree and spends more time in the trees than on the ground, and especially more time in the top part of the trees.

    Well, because of the tree disease, the reproduction rate of Phenotype A is decreased by only 50%, and that of B by 75%.

    Hence, by DEFINITION, Phenotype A is more “fit.” Q.E.D.

    Something is wrong here, isn’t it?

  9. 9
    hammaspeikko says:

    PaV et al, no, the fittest are not the ones who survive. Even the less fit can survive. Fitness is nothing more than a measure of differential rates of reproduction amongst individual in a population. Phenotypes that pass along their genes to subsequent generations at a higher rate than other phenotypes is more fit than the other phenotypes. It can only be determined after the fact. This really is evolution 101 stuff.

    Selection always increases fitness, even in a rapidly declining population. If there is no phenotype linked differential reproduction, there is no selection.

    Well, because of the tree disease, the reproduction rate of Phenotype A is decreased by only 50%, and that of B by 75%.

    Hence, by DEFINITION, Phenotype A is more “fit.” Q.E.D.

    Something is wrong here, isn’t it?

    No. You are exactly correct. Phenotype A’s reproductive rate is higher than phenotype B’s. Therefore it is more fit. Fitness has nothing to do with whether or not the population as a whole is increasing or decreasing.

    Andrew:

    It almost sounds like natural selection (whatever animates it) has a preference for Life.

    No preference at all. Whether or not selection has occurred is based on the outcome, not any past desire.

  10. 10
    PaV says:

    hammaspeiko:

    No. You are exactly correct. Phenotype A’s reproductive rate is higher than phenotype B’s. Therefore it is more fit. Fitness has nothing to do with whether or not the population as a whole is increasing or decreasing.

    This makes “fitness” a completely meaningless term.

  11. 11
    asauber says:

    Whether or not selection has occurred is based on the outcome, not any past desire.

    This makes “selection” a completely meaningless term, since you’re telling me there’s no selection criteria, just a post facto label.

    Andrew

  12. 12
    hammaspeikko says:

    PaV:

    This makes “fitness” a completely meaningless term.

    How so? It can result in a phenotype becoming quickly fixed in a population even if the population is declining. That is all selection “promises”. Remember. Evolution 101.

    Andrew:

    This makes “selection” a completely meaningless term, since you’re telling me there’s no selection criteria, just a post facto label.

    Are you suggesting that post facto labels are meaningless?

  13. 13
    PaV says:

    hammaspeikko:

    How so? It can result in a phenotype becoming quickly fixed in a population even if the population is declining. That is all selection “promises”. Remember. Evolution 101.

    How so?

    I would think this would be evident to you. “Fitness” is, according to what you’ve just written, disconnected from the normal definition of “fitness.” Per your usage, “fitness” is an equivocal term.

    IOW, here’s what you’re saying: “‘Fitness’ means that an organism becomes more vigorous and well-adapted to its environment–as evidenced by its higher reproductive rate. That is, unless it becomes less vigorous, and less well-adapted to its environment though still enjoying a higher reproductive rate.”

    This is rubbish, no?

  14. 14
    asauber says:

    Are you suggesting that post facto labels are meaningless?

    I’m observing the word “selection” is rendered meaningless when it doesn’t mean a selection process with selection criteria and evaluation.

    Andrew

  15. 15
    hammaspeikko says:

    PaV and Andrew, I really don’t understand your confusion. Selection is nothing more or less than a change in allele frequency within the population. This can occur when populations are growing, remain stable, or decline.

  16. 16
    PaV says:

    hammaspeikko:

    I’m sure you’ve read your share of books. We here at UD have also read our share of books. That doesn’t mean we accept as proven, or reasonable, all that’s found there.

    For example, eight years ago we had a discussion here about Biston bistuleria, the peppered moth. It was in the news at the time. One of the regular UD posters, a UD supporter, said he had taken an online course given by a Berkeley professor, and that natural selection is all about “changing allele frequency.” You sound just like this poster.

    Well, I disagreed. I had serious doubts about the whole notion of “changing allele frequencies.”

    Now the ‘peppered moth’ is an ‘icon of evolution.’ This is what Darwinists point to when defending and validating their theory.

    Within the last few months a study came out on Biston bistuleria. It turns out that what caused the transition from the ‘dark’ to ‘light’ form was a transposon located within an intron.

    Now ‘introns’ are normally classified as part of “junk DNA.” And, on top of that, it has been known since the 40’s that ‘transposons’ exhibit ‘non-random’ behavior. So, the ICON of “changing allele frequencies” turns out to be a ‘transposon’ finding its way into some “junk DNA”–that is, a non-random change affecting non-coding DNA. Isn’t that about as far away from “changing allele frequencies” as you can get?

    Reading to us from books won’t carry the day here at UD. Nice sounding words aren’t the same thing as ‘proof.’

    And there is no ‘proof’ for “changing allele frequencies”; at least not in the case of the ‘poster child’ of such assertions.

    Now, what about the demonstrated incoherence of the term “fitness”?
    Don’t you see how vacuous a term it is?

    The lesson of the ‘peppered moth’ study is this: you can run, but you can’t hide. That is, now that whole genome analysis is being done on a grand scale, we’ll actually end up knowing what really goes on within the genome. My prediction has been, and continues to be, that Darwinism cannot hold up to what will be found. And neutral drift is but the next idea to be shut down by genomic studies.

  17. 17
    hammaspeikko says:

    PaV:

    And there is no ‘proof’ for “changing allele frequencies”; at least not in the case of the ‘poster child’ of such assertions.

    I have not read the article on peppered moths, so I can’t comment on it. But the literature is full of examples of changes in allele frequency. Lenski’s experiment is just one.

    Now, what about the demonstrated incoherence of the term “fitness”?

    You have demonstrated no such thing. Fitness “describes individual reproductive success and is equal to the average contribution to the gene pool of the next generation that is made by individuals of the specified genotype or phenotype.” (Wiki) It is relative to the entire population and is independent of the change in size of the population.

  18. 18
    wd400 says:

    I have not read the article on peppered moths, so I can’t comment on it. But the literature is full of examples of changes in allele frequency. Lenski’s experiment is just one.

    The Peppered moth case is another, at least for people that understand what the words “change”, “allele” and “frequency” mean.

  19. 19
    asauber says:

    change in allele frequency within the population

    Just because some sciencey words are stung together doesn’t mean they’ve explained anything.

    Andrew

  20. 20
    hammaspeikko says:

    Andrew:

    Just because some sciencey words are stung together doesn’t mean they’ve explained anything.

    So you don’t have a cogent argument against what I have said. Good to know.

  21. 21
    asauber says:

    So you don’t have a cogent argument against what I have said.

    I’ve already laid it out in simple terms in my above comments, and you’ve chosen to not address it.

    So I ask, just to be polite, what are the selection criteria in natural selection?

    Andrew

  22. 22
    PaV says:

    hammaspeiko:

    But the literature is full of examples of changes in allele frequency. Lenski’s experiment is just one.

    Most everyone in the ID camp accepts the idea and notion of ‘microevolution,’ but the Darwinian idea that ‘macroevolution’ is simply microevolution elongated over time is something that is not proven, and suspect. That’s the basic argument.

    Lenski’s experiment might, in fact, prove that “allele frequencies” change; but it doesn’t enjoy the status that Kettlewell’s experiment still enjoys in biology textbooks. And it turns out to be anything but a “change in allele frequencies.”

    Modern biology is now leading us in the direction of “directed mutations,” a la James Shapiro, which, then, undercuts traditional Darwinian thinking.

    Intriguingly, Darwinists have problems defining ‘species,’ ‘alleles,’ and ‘fitness.’ Not a good sign for a theory that says “changing allele frequencies can eventually lead to the rise of new species through changes in fitness.”

  23. 23
    PaV says:

    wd400:

    The Peppered moth case is another, at least for people that understand what the words “change”, “allele” and “frequency” mean.

    Yes, you’re right. In the hands of evolutionary biologists I don’t know what these words mean; but, that’s because in the hands of evolutionary biologists they ‘mean’ whatever they want them to mean: IOW, they are ‘weasel words’.

  24. 24
    hammaspeikko says:

    PaV:

    Yes, you’re right. In the hands of evolutionary biologists I don’t know what these words mean; but, that’s because in the hands of evolutionary biologists they ‘mean’ whatever they want them to mean: IOW, they are ‘weasel words’.

    These words are very clearly defined and clearly understood by everyone but you and Andrew apparently.

  25. 25
    wd400 says:

    I don’t think any of these definitions are very hard to grasp.

    Allele: One of several versions of a gene. In the peppered moth there is a gene, carbonaria that has two major variants. One that contains a transposon and generates black wings, one that has no transposon and makes white wings.

    Frequency: This is what statisticians call the “relative frequency”. The number of observations matching some category divided by the total number of observations.

    Change: The standard definition. The black-wing allele was formed by a single transposon integration, so the initial frequency was 1/N. Over a few decades it had become very common. The rise in the black winged phenotype is thus explained by the change in the frequency of the black-wing locus.

  26. 26
    PaV says:

    wd400:

    The black-wing allele was formed by a single transposon integration, so the initial frequency was 1/N.

    So, it wasn’t a “change in allele frequency,” it was a completely unanticipated change: which I’ve been saying all along.

  27. 27
    PaV says:

    hammaspeiko:

    These words are very clearly defined and clearly understood by everyone but you and Andrew apparently.

    I’m afraid not. “Allele” is a fluctuating concept, as wd400 has just demonstrated.

    And “fitness” is a meaningless concept in this regard: in the hands of evolutionary biologists, “fitness” is a like a sign alongside a road. It points in a direction, and says, “Fitness in this direction.” The only problem is that there isn’t just one, single sign, but, hundreds of them, all saying the same thing–“fitness in this direction”, and pointing in every possible direction. And, so, evolution always “increases fitness,” no matter what direction it’s going. Meaningless. And the fact that you can’t see this problem dooms you to holding on to an incoherent theory.

  28. 28
    wd400 says:

    What has anticipation to do with anything? Alleles are created by mutation, when they enter the population they have a frequency of 1/N (where N is the number of individuals, so 1/2N genes in diploids like these moths).

    I am genuinely lost as to what your problem is here.

  29. 29
    hammaspeikko says:

    WD400:

    I am genuinely lost as to what your problem is here.

    As am I. The concept is very simple.

  30. 30
    PaV says:

    wd400 and hammaspeikko:

    I agree: you’re both lost.

  31. 31
    Bob O'H says:

    PaV @ 26 – that’s only not a change if 0 = 1/N. Also, what happened afterwards was also a change in frequency.

    wd400 & hammaspeikko – maybe this paper will help.

  32. 32
    PaV says:

    Bob O’H:

    When the “change” occurs in an intron and not an exon, then the normal defintion of what constitutes an “allele” has been violated.

    IOW, you’ve elevated “junk DNA” to the level of an “allele.” You can do whatever you like; just don’t call it science.

  33. 33
    Bob O'H says:

    PaV – why? The change in the intron changes the function, and hence thus the phenotype. Thus you have a different allele. That’s all that matters.

  34. 34
    critical rationalist says:

    Knowledge is information that plays a causal role in being retained when embedded in a storage medium. In the case of biological organisms, this means playing a causal role in being copied into the next generation. The reduction of an organism’s fitness is not incompatible with this.

    Take a hypothetical island with a hypothetical species of bird. Currently this species nests in May, which is optimal for the islands climate and food supply. However, due to the islands geography, not all nesting areas are equal in that some are significantly farther from food, more exposed to predators, etc.

    Now, hypothetically, one of these birds is born with a mutation that causes it to nest in April, which is a month earlier. As such, it gets the best nesting location. It also finds a suitable mate and has offspring, which also inherit this same mutation. While being born a month early is a sub optimal for the island’s climate and food supply, this is outweighed by the fact that they have the best nesting location. Next season, their offspring also nest earlier, obtain the best nesting locations, etc. This continues until eventually the early nesting mutation has spread throughout the entire population, which has made it less fit as a whole.

    If a bird is born with a mutation to nest a month later, which would again represent the optimal time, all of the best nesting locations would already be taken. The mutation would not spread thought the population. However, if a bird is born with a mutation to nest yet another month earlier, the process would repeat itself. This would results in the entire population is even less fit. These birds have a harder life, find it more difficult to find food, because there is less of it at this time, and are generally less fit than the birds that nest in May. Nesting earlier only serves to cause the earlier nesting genes to make it into the next generation.

    At some point, mutations to nest earlier would eventually prove lethal to offspring. As such, if all things remain equal, there is a minimum level of fitness the entire species would maintain. But, this could still be far from the original fitness the species first exhibited. However, if the climate suddenly changes, such as cold weather last significantly longer in a season, the entire species could go extinct.

    So, rather than merely being “the survival of the fittest”, we say that genes are biological replicators, in that they play a causal role in their own replication by their environment. Furthermore, we include the organism itself as part of the gene’s environment. As such, it’s the genome itself that becomes better adapted to be replicated by it’s environment – even potentially at the expense of the organism becoming less fit as a whole.

  35. 35
    wd400 says:

    When the “change” occurs in an intron and not an exon, then the normal defintion of what constitutes an “allele” has been violated.

    The term pre-dates the discovery that DNA was the genetic material, let alone the structure of protein coding genes in eukaryotes. This other definition of allele seems to exist only in your head.

  36. 36
    PaV says:

    Bob O’H:

    The change in the intron changes the function, and hence thus the phenotype. Thus you have a different allele. That’s all that matters.

    Not really. It is a kind of verbal ‘slight of hand’. The common understanding of an ‘allele’ is that it represents some different form of a gene, and that that gene produces some kind of protein.

    So the common understanding is that an ‘allele’ is a variant protein form, and that that in turn is responsible for phenotypic variation. So, e.g., from Wikipedia:

    Genes can acquire mutations in their sequence, leading to different variants, known as alleles, in the population. These alleles encode slightly different versions of a protein, which cause different phenotypical traits.

    But something entirely different is happening here, and you’re simply subsuming it under the term ‘allele’. The ‘intron’ does not show up in the actual form of the protein. This is not honest science. And it allows population geneticists to not have to deal with the consequences of what is actually happening here.

  37. 37
    PaV says:

    wd400:

    This other definition of allele seems to exist only in your head.

    No, it actually exists in those peppered moths.

    Words, on the other hand, can be played with, as in, e.g., “It all depends on what the definition of is is.”

  38. 38
    wd400 says:

    And it allows population geneticists to not have to deal with the consequences of what is actually happening here.

    Again, “what is happening here” is that a genetic varaint (allele) was formed (by insertion of a transposon). That variant had a phenotypic effect that increased the reproductive success of its bearers. As a result the variant raised from a very low frequency to a high one.

    So. Again. Can you please spell out the difficulty you are having here?

  39. 39
    Bob O'H says:

    PaV –

    Not really. It is a kind of verbal ‘slight of hand’. The common understanding of an ‘allele’ is that it represents some different form of a gene, and that that gene produces some kind of protein.

    The first part of the common understanding is broadly correct, depending on how broadly you define a gene (some sequences that affect the regulation of a protein-coding gene can be a long way from that gene. So they will be IDed as different genes). Technically, we tend to talk more about “loci”, rather than “gene” in many contexts, because what we are looking at could be many things, including neutral genetic markers, and even they have alleles.

    So the common understanding is that an ‘allele’ is a variant protein form, and that that in turn is responsible for phenotypic variation.

    And this is wrong – when genetics was developed, we didn’t even know that DNA was the genetic material, so we had no idea what alleles actually were. And for a lot of work in genetics it doesn’t matter, e.g. we can still map loci that affect traits like disease resistance in wheat, without knowing what the resistance gene is or does, and this is still useful for breeding better wheat varieties.

    I don’t know which Wikipedia page you’re citing (update: ah, it’s ‘gene’), but it’s not the page on allele, and if you read it carefully, you’ll see that it doesn’t define ‘allele’, it say that gene variants are called alleles, but doesn’t say anything about other types of locus having alleles.

    BTW, how do you know that the carbonaria allele isn’t the result of a change in the protein encoded by cortex? From the reports it’s clear that they didn’t know the mode of action of the gene, and they haven’t published anything on it since then.

  40. 40
    PaV says:

    wd400:

    Again, “what is happening here” is that a genetic varaint (allele) was formed (by insertion of a transposon). That variant had a phenotypic effect that increased the reproductive success of its bearers. As a result the variant raised from a very low frequency to a high one.

    But, as we’ve discussed before, transposons are NOT random; and, “junk DNA” was not considered essential to species formation. So, non-randomness, and supposedly “dead” DNA, are what give rise to what we see.

    Let’s remember that when “changing allele frequencies” are invoked, it is thought of as natural selection eliminating less “fit” “alleles,” and thus disturbing the presence of the ‘unfit’ allele in its population.

    But this is a completely different mechanism. And the lack of “randomness” is swept under the carpet. And the fact that “junk-DNA”= intron is involved means that we’re seeing a change in allelic expression, NOT “changing allele frequencies.” We can lie by commission; or by omission.

  41. 41
    PaV says:

    Bob O’H:

    When everything is ill-defined, then you don’t really know what’s going on.

    Distinctions need to be made. A different vocabulary developed, but one that “maps” to something real.

    From Wikipedia’s page on Kettlewell’s Experiment:

    The conclusion of Kettlewell’s experiment can be summarised as follows:[10][13]

    1. Birds were the main predators of moth.

    2. Moth were eaten by birds selectively in both polluted and clean forests, indicating camouflage efficiency of the different varieties of moths.

    3. The more conspicuous form of moth was always less in number after recapture; i.e. the white type in Birmingham, and the black type in Dorset.

    4. In clean and lichened area, dark moths remained scarce and were rapidly eliminated because of their conspicuousness even when experimentally introduced.

    So, what happened exactly? According to implicit Darwinian expectations, allele A began to be favored, and so allele B began to disappear.

    But that’s not what happened. What happened was allele C appeared! And, it began to be favored.

    Did the moths get together and say: “Look, we’re getting wiped out. We stand out too much against the light background of these trees. We got to do something”?

    No. Its genome changed. What is important here is HOW “allele C” arose. And it arose “non-randomly.” That’s the “news.” But, no, not according to population geneticists. According them it was nothing more than “changing allele frequencies,” with this “new” allele have a frequency of 1/N. Ho-hum.

    Alan Shepherd is sent up on a rocket into low earth orbit, and then returns.

    Ho-hum: “what goes up, must come down.”

  42. 42
    wd400 says:

    But, as we’ve discussed before, transposons are NOT random; and, “junk DNA” was not considered essential to species formation. So, non-randomness, and supposedly “dead” DNA, are what give rise to what we see.

    Transposon intergration is random with respect to fitness: they aren’t generating useful alleles on demand. That should be obvious in this case because all black moths inherited their black-wing allele from a single event. What kind of programmed response occurs once in thousands upon thousands of moths exposed to the same stimulus.

    Let’s remember that when “changing allele frequencies” are invoked, it is thought of as natural selection eliminating less “fit” “alleles,” and thus disturbing the presence of the ‘unfit’ allele in its population.

    Yes. That’s what happened here.

    And the fact that “junk-DNA”= intron is involved means that we’re seeing a change in allelic expression, NOT “changing allele frequencies.” We can lie by commission; or by omission.

    I’m afraid this is hardly English, let alone a cogent scientific statement. Again, an allele went from a very low frquency (just one copy!) to a very high one. The fact the allele is intronic really has no special meaning.

    In science “allelic expression” means allele-specific rates of RNA production from genes. I don’t see how allelic expression could conflict with changing alelle frequencies, so I suppose you meant something different by the term?

    No. Its genome changed. What is important here is HOW “allele C” arose. And it arose “non-randomly.”

    What evidence do you have for this claim? If it arose non-randomly why did it only arise once?

  43. 43
    PaV says:

    wd400:

    Transposon intergration is random with respect to fitness: they aren’t generating useful alleles on demand. That should be obvious in this case because all black moths inherited their black-wing allele from a single event. What kind of programmed response occurs once in thousands upon thousands of moths exposed to the same stimulus.

    There’s a very simple answer to this question–and it’s likely, in the long term, to be the correct one. The “programmed response” happens to be “random.” Nevertheless, this “programmed response” is “triggered” by the environment, and, hence, ultimately “non-random.” This is just the behavior McClintock was observing 60 years ago.

    You don’t have to live in an “either-or” world.

    I’m afraid this is hardly English, let alone a cogent scientific statement.

    Why do I have to spell everything out for you?

    If we’re dealing with an “intron”, then we’re not dealing with a different form, or ‘allele,’ of the original protein; that only leaves ‘regulation of expression’ as the avenue of bringing about phenotypic changes. And putative “junk DNA” is seen over and over again to have regulatory function.

    In science “allelic expression” means allele-specific rates of RNA production from genes. I don’t see how allelic expression could conflict with changing alelle frequencies, so I suppose you meant something different by the term?

    No, I mean precisely what “allelic expression” means.

    What I don’t understand is this conclusion of yours: “I don’t see how allelic expression could conflict with changing allele frequencies. . . ” To consider process A, and process B to be basically the same process because they bring about the same result is, as I said above, to fail to make proper distinctions because differences do remain. Is wind erosion the same as water erosion? OTOH, yes: soil is eroded. But, OTOH, it’s not the same because the process isn’t the same, and while both lead to erosion, wind-eroded outcrops look different than water-eroded outcrops.

    What evidence do you have for this claim? If it arose non-randomly why did it only arise once?

    From:Genome-wide characterization of non-reference transposons in crops suggests non-random insertion, which is found here.

    In recent years, we have gradually realized the importance of transposons in genome structure, function and evolution. As a fundamental function elements constituting the genomes, transposons are playing important roles in the formation and evolution of the DNA “jigsaw puzzle” structure. They are distributed nonrandomly in large genome and have a correlative relation between other function elements [7, 8]. Transposons not only affect plant genome structure but also play important roles in gene expression regulation [9]. Their activity can inactivate genes. Some transposons prefer insertion into genes or near gene flanking regions, leading to a mutation that affects gene function. This transposon activity can be engineered using appropriate vectors to produce artificial mutations in genes. For example, wrinkled peas result from a 0.8-KB transposon insertion in the SBE1 gene, the mechanism of which is similar to the mechanism for the corn Ac/Ds transposon family [10]. Transposon insertion can also positively or negatively alter gene expression levels. A classic example is the transposon insertion into intron 1 of the maize knotted1 gene, causing the expression in the leaves [11]. In additional, transposon insertions can also cause gene rearrangement and epigenetic silencing.

    Doesn’t all of this sound familiar?

  44. 44
    wd400 says:

    There’s a very simple answer to this question–and it’s likely, in the long term, to be the correct one. The “programmed response” happens to be “random.” Nevertheless, this “programmed response” is “triggered” by the environment, and, hence, ultimately “non-random.” This is just the behavior McClintock was observing 60 years ago.

    You don’t have to live in an “either-or” world.

    I mean… I really think we do in this case.

    No, I mean precisely what “allelic expression” means.

    What I don’t understand is this conclusion of yours: “I don’t see how allelic expression could conflict with changing allele frequencies. . . ” To consider process A, and process B to be basically the same process because they bring about the same result is, as I said above, to fail to make proper distinctions because differences do remain. Is wind erosion the same as water erosion? OTOH, yes: soil is eroded. But, OTOH, it’s not the same because the process isn’t the same, and while both lead to erosion, wind-eroded outcrops look different than water-eroded outcrops.

    I guess this is a little helpful in finding the source of your confusion. Of course the intronic variant is not changing the protein (so there is no alternative protein isoform). But the allele does does change the expression levels of the gene and so the amount of protein in the cell and particular times.

    So, we have an allele (a genetic variant) that has a molecular phenotype (regulation of gene expression) which generates a physical phenotype (black wings). The fact the molecular basis of the physical phenotype is a change in gene expression and not a change in protein sequence in neither here nor there when it comes to your original claim that “chaning allele frequenceis is far as you can get” from the peppered moth example.

    Doesn’t all of this sound familiar?

    Certainly your tendency to scan abstracts for words you think support your case is familiar. When these authors so the transposon intergration is “non-random” that are not talking about being able to generate particular traits. They mean the distribution of elements across genomes and with respect to genes is not uniformally random. This partially a result of selection removing transposons, and partly a result of some element’s tendency to insert into other copies of their own sequence. In this case they take the extra step of looking only allelic variants (i.e. transposon copies that are the result of recent activity and not accumulation of ancient events).

    There is no doubt that repetitive elements are a source of gene regulatory mutations (I am writing a paper documenting a examples this right now!). But when a transposon integrates that creates a new allele. Whatever the effects of that allele, it will act like any other. Selection, drift and recombination will influence its future.

  45. 45
    PaV says:

    wd400:

    I guess this is a little helpful in finding the source of your confusion. Of course the intronic variant is not changing the protein (so there is no alternative protein isoform). But the allele does does change the expression levels of the gene and so the amount of protein in the cell and particular times.

    The “confusion” is on your part. Here’s part of the defintion of “confusion” (Merriam Webster):

    Word Root of confusion
    The Latin word fundere, meaning “to pour,” and its form f?sus give us the roots fund and fus. Words from the Latin fundere have something to do with pouring. To refund is to pour someone’s money back to her or him. Confusion exists when too many things are poured together so that they become uncertain and unclear.

    You equate a mutation in an exon leading to a different form of a protein to something that is a completely different process, not only in how it arises, but how its effects are produced. This is literally “confusion.” And you persist in it.

    Or, as you put it:

    The fact the molecular basis of the physical phenotype is a change in gene expression and not a change in protein sequence is neither here nor there when it comes to your original claim that “changing allele frequencies is far as you can get” from the peppered moth example.

    Which gets us back to my earlier comment:

    No. Its genome changed. What is important here is HOW “allele C” arose. And it arose “non-randomly.” That’s the “news.” But, no, not according to population geneticists. According them it was nothing more than “changing allele frequencies,” with this “new” allele have a frequency of 1/N. Ho-hum.

    Alan Shepherd is sent up on a rocket into low earth orbit, and then returns.

    Ho-hum: “what goes up, must come down.”

    Neither here nor there.” Indeed, “ho-hum.

    Certainly your tendency to scan abstracts for words you think support your case is familiar. When these authors so the transposon intergration is “non-random” that are not talking about being able to generate particular traits. They mean the distribution of elements across genomes and with respect to genes is not uniformally random. This partially a result of selection removing transposons, and partly a result of some element’s tendency to insert into other copies of their own sequence.

    I’ve read parts of Barbara McClintock’s original paper on transposons. The places where transposons insert themselves are not random. In the paper I cited, they state rather unequivocally that transposons tend to insert themselves in “introns.”

    To lay the “non-random” effects of transposon insertion totally on NS, is to be a “true believer.” You don’t do that. But I think you want to imply that.

    There is no doubt that the inner workings of living cells is something extraordinary. There is no doubt that part of these inner workings utilizes ‘randomness.’ But there is something purpose-driven, i.e., teleological, that we can glimpse in these inner workings, and I think that’s something you prefer not to look at.

    Here at ID, it’s something we pay extra attention to. And, you know what, in time we’ll be proved right, and you will be proved wrong. Completely wrong? No. You will be proved wrong in the kind of emphasis you put on ‘randomness.’

    Time will tell.

    And, BTW, good luck with your paper.

  46. 46
    PaV says:

    wd400:

    But when a transposon integrates that creates a new allele. Whatever the effects of that allele, it will act like any other. Selection, drift and recombination will influence its future.

    I don’t much problem with this statement. And I’m more reluctant than almost anyone else at UD to accept neo-Darwinism; so, this isn’t really an issue for those who hold to Intelligent Design.

    Rather, what is at issue is how variations arise. That’s the whole question. IOW, as someone has coined the term: it’s not the ‘survival of the fittest,’ it’s the ‘arrival of the fittest.’ That’s where we’re pages apart.

    I think that at some time in the future–and it might be distant–we will discover that environmental cues cause the cell’s machinery to allow certain portions of its genome to mutate at a higher rate in a purposeful and engineered fashion. A bullet fired by a rifle is a powerful thing: it can easily kill someone; but, it can’t lift someone into outer space. My analogy of “micro-” and “macro”-evolution.

    I just had cataract surgery in both eyes. They placed artificially made lenses in both eyes. Those lenses were manufactured to have precise qualities, just like the natural lenses they were replacing. Now, tell me, did “random” variations and selection lead to those replacement lenses; or, were they the result of purposeful action by intelligent agents?

    “Ay, there’s the rub.”

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