-
Welcome to Religious Forums, a friendly forum to discuss all religions in a friendly surrounding.
Your voice is missing! You will need to register to get access to the following site features:- Reply to discussions and create your own threads.
- Our modern chat room. No add-ons or extensions required, just login and start chatting!
- Access to private conversations with other members.
We hope to see you as a part of our community soon!
Creationists, please provide evidence
- Thread starter evolved yet?
- Start date
newhope101
Active Member
No just bored repeatedly having to tell you you're jumping the shark again.
Just wolfjumping
This experiment had nothing to do with making a new "kind" of anything... they were seeing if the flies would develop faster. You are once again offering up a paper that has nothing to do with what you think it does.
I did not say the researchers were trying to make new kinds. They were trying to fix an advantageous allele for 'accelerated development' into the fruitfly population. They didn't. Further they say advantageous allele fixation would be even more difficult in the wild away from controlled conditions. They are looking for more than phenotypic changes. They are looking for single nucleotide polymorphism changes and found "little allele frequency differentiation'. This type of fixation is what is required for eventual macroevolution change.
wa:do
The research speaks to the inability of an advantageous allele to become fixed in the population of fruitfly. The advantageous allele is 'accelerated growth'.
What happened? This allele did not become fixed.
What does this mean to me? I do not expect these researchers were trying to fix this advantageous allele in their experiment because they were bored. I can safely assume that these researchers were hoping or wondering if this allele would fix in the population. That's why they were looking for allele fixation...hey hey..?? What do you think they were doing PW?
Why? it would have been another support for evolution if these researchers could show changes at more than the phenotypic level, as well as headlines. Why? because so far they haven't.
Similarly with the fruitflys adaptation to climate change research... Do you think these researchers were just wasting their time again here? I think they were not. Rather, they were seeing if these fruitflys could adapt to climate change. They didn't. The research sites lack of variation ability. The fruitfly were limited in their ability to adapt. This reseach is clear in what it says, also.
600 generations, one would expect some fixation going on of this advantageous allele. It didn't happen. This is something researchers can see, rather than assume.
I do not think it is I that cannot interpret the research. Unfortunately it is you. You appear unable to discern that the advantageous allele is the 'accelerated development' allele. That is what did not become fixed.
Are you having trouble interpreting the research or are you misrepresenting it intentionally, again?
David M
Well-Known Member
No its not evidence for your spurious claim.
Did you read that abstract? The one that specifically stated that there was both faster development and changes in phenotype as well as differences in allele frequency, the populations evolved. Nothing in this study shows that changes will never reach fixation.
It is well known that unconditionally advantageous mutations are rare, that most advantageous mutations are only slightly advantageous and that fixation can take a long time.
However much you would like to deny it this study showed phenotype changes in populations after 600 generations.
You might expect it, but then that is the sort of rate of evolution only required by people who think that multiple species evolved from each of the "kinds" that Noah took on the ark.
People who actually understand evolution would not expect fixation over such a short period.
Well you are wrong there.
Nope, but you are, again.
Last edited:
tumbleweed41
Resident Liberal Hippie
So then, you have no coherent response to my questions?
painted wolf
Grey Muzzle
No, an allele is a particular gene... "accelerated growth" is a phenotype.
This phenotype is likely polygeneic and they talk about multiple alleles.
Do you understand what fixation means?
It means that the particular allele completely replaces the other alleles of the same gene. If the allele is dominant then it may never fix because other alleles can hide in the heterozygus condition. The phenotype however can still become the "fixed" evolved expression.
I think they were exploring how whole genomic variation in sexual large genome population varies from asexual small genome populations. They say so in the first sentence.
Abstracts are written to get across the most information possible in the shortest number or words possible... the first sentence tells you the purpose of the experiment.
No, they were comparing how different sexual species are from asexual species.... sexual species are more complex in how genetic change is inherited.
This is another paper that confirms that overspecialization is a problem for species... and that the tropics are not as nice to species because overspecialization is rife. Overspecialization results in limited gene pools and thus lower genetic variability... this paper is just more confirmation for that. You will notice they were talking about a very specalized species of fruitfly... not a generalist species.
If you actually did any work in this area then you would not be surprised. Again, if the trait is heterozygus dominant and in a sexually reproducing species then fixation is all but impossible.
This is why it is going to be impossible to get rid of Sickle Cell Disease... it will always hide in the population in the heterozygus condition.
No really... it is that you can not interpret the research... you simply don't have the knowledge base to understand what is being discussed.
You fixate on certain words and then make odd logical jumps based on what limited knowledge you have.
The problem is that you feel your conclusions are totally valid no matter what other information is presented to you.
No... I actually have the knowledge base to know what is being discussed. I've done fixation experiments.
wa:do
newhope101
Active Member
Paintedwolf the researchers looked for evidence of a “selective sweep” – the signature of a beneficial mutation becoming fixed in the population – and could not find it. They did the selection artificially, forcing the fly embryos to evolve toward faster embryonic development. Despite lots of mutations, they found the flies resistant to change. Not only that, the flies underwent “reverse evolution” – they said, “forward experimental evolution can often be completely reversed with these populations, which suggests that any soft sweeps in our experiment are incomplete and/or of small effect” (a soft sweep meaning selection is acting on standing variation instead of new mutations). Possibly any beneficial mutations were hindered by linked deleterious alleles (canceling out the benefit) or antagonistic pleiotropy (in which one good mutation to a gene can cause one or more bad effects elsewhere). Either way, the evolution is like one step forward, one or more steps back.
There was even more bad news for neo-Darwinian theory: the lab situation was more optimistic than the wild, where adaptive evolution is expected to occur. You can get a lot of variation and mutation to appear in genomes, but no unconditionally beneficial mutations. Their last paragraph expressed surprise at this, with a subtext of disappointment:
"Our work provides a new perspective on the genetic basis of adaptation. Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments. This suggests that selection does not readily expunge genetic variation in sexual populations, a finding which in turn should motivate efforts to discover why this is seemingly the case".
This experiment was begun in 1975. After 35 years and 600 generations, accelerated by artificial selection, the net evolution (in terms of adaptation and improvement in fitness) was negligible if not nil.
Have you got anything else to say PW? Perhaps you could inform these researchers as to why sexually reproducing organisms do not lead to the fixation of advantageous alleles in non sexually reproducing organisms. Perhaps you need to review phenotype and mitochondrial mutations.
The point I made stands. After 600 generations the advantagious allele was not fixed and 'fitter' adaptations did not occur in the population. Adaptation is one of your major concepts to invoke macrevolution eventually. This supports the concept that adaptation is not working as your leading researchers thought it would in sexually reproducing organisms. Otherwise they would not have recommended someone look into WHY. Get it?
There was even more bad news for neo-Darwinian theory: the lab situation was more optimistic than the wild, where adaptive evolution is expected to occur. You can get a lot of variation and mutation to appear in genomes, but no unconditionally beneficial mutations. Their last paragraph expressed surprise at this, with a subtext of disappointment:
"Our work provides a new perspective on the genetic basis of adaptation. Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments. This suggests that selection does not readily expunge genetic variation in sexual populations, a finding which in turn should motivate efforts to discover why this is seemingly the case".
This experiment was begun in 1975. After 35 years and 600 generations, accelerated by artificial selection, the net evolution (in terms of adaptation and improvement in fitness) was negligible if not nil.
Have you got anything else to say PW? Perhaps you could inform these researchers as to why sexually reproducing organisms do not lead to the fixation of advantageous alleles in non sexually reproducing organisms. Perhaps you need to review phenotype and mitochondrial mutations.
The point I made stands. After 600 generations the advantagious allele was not fixed and 'fitter' adaptations did not occur in the population. Adaptation is one of your major concepts to invoke macrevolution eventually. This supports the concept that adaptation is not working as your leading researchers thought it would in sexually reproducing organisms. Otherwise they would not have recommended someone look into WHY. Get it?
Last edited:
painted wolf
Grey Muzzle
First... if you are going to quote you need to cite your source... plagiarism is against the rules.
Creation-Evolution Headlines
Did you bother to try to understand anything I said in my previous post? Or are you just going to continue to plagiarize others to fake it?
Nothing in your plagiarized words refutes anything I said about the research.
wa:do
newhope101
Active Member
PW.....Are you hoping that no one can understand some basics of this research? It is fairly clear. 600 generations ...no allele fixes. Any benefit is found by the interplay of genes.
The point still being little if any allele change was found. That's it.
The point still being little if any allele change was found. That's it.
Last edited:
newhope101
Active Member
Generational research on drosophila sheds light on genetic mechanism of evolution
November 1, 2010 by Janet Wilson
In fact, humans and fruit flies share 70 percent of the same genes, making us closer cousins than we might think. Now, with data from 600 generations of fruit flies, Burke and two UCI professors have addressed a question that has long bugged scientists.
For years, evolutionary biologists have dickered over whether sexual beings – including fruit flies and humans – evolve in the same way as asexual yeast and bacteria. The researchers say they’ve proved the answer is an emphatic no. It would seem to be esoterica only a scientist could appreciate. But ecology & evolutionary biology professor Michael Rose says the conclusion, reported recently in the journal Nature, could fundamentally alter the quest for new pharmaceuticals and other products.
Beginning in 2009, Burke ground up Rose’s fly populations – both the “live fast” and control-group varieties – into genetic soups. After computers untangled their long streams of DNA, she pored over all of the flies’ 14,000 sets of genes, looking for any variations linked to faster development. Burke found not one instance of a single gene spreading quickly. But she isolated more than 500 genes associated with sped-up development.
The experiment, Rose says, “is a total vindication of Wright and Fisher and a major defeat for Haldane and a lot of conventional geneticists who have sided with him.”
Not so fast, says noted evolutionary biologist Richard Lenski of Michigan State University: “There are cases where a single gene affects something. But here’s an example of rigorous research that really reveals just how complex some of these genetic traits can be.”
Rose points out that if human disease is controlled by many genes, it would explain the difficulty in creating completely safe drugs. Side effects, for instance, are probably caused by medications targeted at a single gene, without taking into account other responsible genes.
Wiki Population genetics
The work of Fisher, Haldane and Wright founded the discipline of population genetics. This integrated natural selection with Mendelian genetics, which was the critical first step in developing a unified theory of how evolution worked.[46][47]
John Maynard Smith was Haldane's pupil, whilst W.D. Hamilton was heavily influenced by the writings of Fisher. The American George R. Price worked with both Hamilton and Maynard Smith. American Richard Lewontin and Japanese Motoo Kimura were heavily influenced by Wright.
　
So basically Fisher and Wright were right. Haldane that also influenced population genetics was wrong. Evolution is not about the alleles and spreading genes but about the interplay of genes and gene expression. This has implications for your algorithms. If it doesn’t, then it should!
The fruit fly’s reverted back in changed environments and no evolution occurred. So after 600 generations no genes became fixed. Some fruit flys developed faster but no DNA changed, just 500 identified genes accociated with it were seen, nothing selected. No evolution happened. No genotypic changes happened. There was in-kind variation, as usual. 600 generations or 6 sqillion generations fruitflies were never bacteria.
November 1, 2010 by Janet Wilson
In fact, humans and fruit flies share 70 percent of the same genes, making us closer cousins than we might think. Now, with data from 600 generations of fruit flies, Burke and two UCI professors have addressed a question that has long bugged scientists.
For years, evolutionary biologists have dickered over whether sexual beings – including fruit flies and humans – evolve in the same way as asexual yeast and bacteria. The researchers say they’ve proved the answer is an emphatic no. It would seem to be esoterica only a scientist could appreciate. But ecology & evolutionary biology professor Michael Rose says the conclusion, reported recently in the journal Nature, could fundamentally alter the quest for new pharmaceuticals and other products.
Beginning in 2009, Burke ground up Rose’s fly populations – both the “live fast” and control-group varieties – into genetic soups. After computers untangled their long streams of DNA, she pored over all of the flies’ 14,000 sets of genes, looking for any variations linked to faster development. Burke found not one instance of a single gene spreading quickly. But she isolated more than 500 genes associated with sped-up development.
The experiment, Rose says, “is a total vindication of Wright and Fisher and a major defeat for Haldane and a lot of conventional geneticists who have sided with him.”
Not so fast, says noted evolutionary biologist Richard Lenski of Michigan State University: “There are cases where a single gene affects something. But here’s an example of rigorous research that really reveals just how complex some of these genetic traits can be.”
Rose points out that if human disease is controlled by many genes, it would explain the difficulty in creating completely safe drugs. Side effects, for instance, are probably caused by medications targeted at a single gene, without taking into account other responsible genes.
Wiki Population genetics
The work of Fisher, Haldane and Wright founded the discipline of population genetics. This integrated natural selection with Mendelian genetics, which was the critical first step in developing a unified theory of how evolution worked.[46][47]
John Maynard Smith was Haldane's pupil, whilst W.D. Hamilton was heavily influenced by the writings of Fisher. The American George R. Price worked with both Hamilton and Maynard Smith. American Richard Lewontin and Japanese Motoo Kimura were heavily influenced by Wright.
　
So basically Fisher and Wright were right. Haldane that also influenced population genetics was wrong. Evolution is not about the alleles and spreading genes but about the interplay of genes and gene expression. This has implications for your algorithms. If it doesn’t, then it should!
The fruit fly’s reverted back in changed environments and no evolution occurred. So after 600 generations no genes became fixed. Some fruit flys developed faster but no DNA changed, just 500 identified genes accociated with it were seen, nothing selected. No evolution happened. No genotypic changes happened. There was in-kind variation, as usual. 600 generations or 6 sqillion generations fruitflies were never bacteria.
tumbleweed41
Resident Liberal Hippie
An allele is one of two or more forms of the DNA sequence of a particular gene.
Biological Evolution is the change over time in the proportion of individual organisms differing in one or more inherited traits. A trait is a particular characteristicanatomical, biochemical or behaviouralthat is the result of geneenvironment interaction. Evolution may occur when there is variation of inherited traits within a population. The major sources of such variation are mutation, genetic recombination and gene flow.
Source
Most of what you paste further explains the mechanisms of biological evolution.
That you do not get this only magnifies your apparent ignorance of biology and biological evolution, and shows a dogmatic adherence to Creationism despite evidence to the contrary.
But what of the OP?
Where is your objective empirical evidence in support of Creationism?
painted wolf
Grey Muzzle
NO... if you bothered to read it you would see that plenty of allele change was found... but not fixation.
You really need to pay attention to what is written.
How do you go from dozens to zero is beyond me.:slap:
wa:do
painted wolf
Grey Muzzle
Do you bother to read anything? This is just a news article about the same experiment you just posted... and it backs up my position!:faint:
You really don't pay attention do you? Evolution is about both how genes spread in the population and how they are expressed. Genotype and Phenotype.
If you payed attention, I and the article you just posted above, mention that things change if you are dealing with polygenic traits or single gene traits.
Lots of genotypic changes happened you dunce.... fixation is not a reflection of genotypic change. They specifically mention over 600,000 changes in the DNA!
500 genes were shown as having influence on faster development and selected for in the dozens of allele changes.... why can't you read?
Yes, the fruit-flies reverted when not under selective pressure to develop faster...that is still evolution. They changed to suit their situation and that was thanks to the fact that there wasn't fixation because the traits are polygenic and likely not all heterozygous. They say so in the article!
They wern't trying to get the flies to "change kinds" and your insistence on this point is more proof of your lack of ability to grasp anything that is going on with the scientific research.
wa:do
newhope101
Active Member
PW and all of you. Kinds were created with the DNA/genes they were created with. Gene families work differently to allow for some adaptation. Fruit fly may invert genes in response to climatic conditions, some do not have the diversity to adapt further. They may mutate more wings, develop quicker, and may be given different species names. They remain the same kind, always were the same kind and will always be the same kind. Wiki Brachycera attests to the confusion within this kind as far as your phylogeny goes.
Your research here in my previous research has shown, same genes, different expression. The allele differences expected by Haldanes assumptions did not arise. Hence evolution, the process of allele change of the genotype did not occur over 600 generations. Yes this was a small time scale comparable to 12,000 years of human evolution. The research itself says this.
There are 135,000 single nucleotide differences and 5 million insertion/deletion events and other chromosomal rearrangements humans have undergone since divergence from the common ancestor. About 27% of the chimp genome does not align with the human genome. The overall genome comparison of 30% difference. Many papers cite 4-6% difference, depending on method. See Wiki Chimpanzee Genome Project.
We’ve had 5-8 my to do it. Hence accelerated evolution is meant to explain a lot of it. Yet the Initial Sequence of the Chimpanzee cited that 9 chromosomes that underwent major changes showed no evidence of accelerated adaptive evolution of chromosomes. The explanations involved terms like ‘may reflect’ and appear vague at best. See Initial Sequence of the Chimpanzee Genome - The Chimpanzee Sequencing and Analysis Consortium*
What I am saying is this research into fruitflys at least gives results you can see. There is still modelling done but the results are more reliable. The research shows so far that there was no sign of even the beginning of major genetic changes. Yes you can say, ‘there was insufficient time to observe these changes‘. Or you could say one to 135 nucleotide change had to occur on average every 5-8,000 years in the human line since divergence to account for the differences in just single-nucleotides.
The fruit fly 600 generations is equivalent to 12,000 years your researchers say. The hoped for comparative change did not occur in a test species. The fruitflies showed undetectable genomic change according to the research. That is science. Your science illustrates evolution, as you see it, is not occurring in this research. In kind variation occurs at no more than an expressive level. This is not the end of the story but is good supportive evidence in the here and now that evolution on a macro level does not occur and that kinds were created individually. Let’s see what happens if they go for another 35 years. There will still be no sign of change at any more than an expressive level.
Evos may interpret data as they wish. I likewise, may do the same.
Last edited:
Autodidact
Intentionally Blank
your first step would have been to state your hypothesis. You didn't. Therefore you haven't posted evidence of anything. Hooray!
painted wolf
Grey Muzzle
How do you get from over 600,000 single nucleotide changes and dozens of new alleles to "not identifying changes"?
Seriously.... how does this work?
What is that creo code for "make stuff up"?
Like jumping from "a part of the Mandibular ramus is gorilla-like" to "has a gorilla jaw"? Your ability to extrapolate is far from being demonstrated logical.
What misquote.... you frequently jump up and down and say "There was in-kind variation, as usual. 600 generations or 6 sqillion generations fruitflies were never bacteria." When the research wasn't about this issue in the slightest.
And what DNA/genes were those? Not all humans have the same genes... many don't have the gene for digesting milk... does this make them less human?
What about when new genes appear in a population? Are they now suddenly a new created kind?
You obviously realize that your much hated algorithms, statistical models and phylogenetic trees are used to determine gene families yes?
Why is it ok here but not for whole genomes?
Which of the 120+ "kinds" are you reffering to? Why was an intelligent designer so caught up with making so many kinds of these flies? Just bored or to uncreative to come up with anything else?
Did you actually read the research? No, you skimmed the abstract. Even in the abstract they say that allele change occurred... dozens of them!
I don't know why you keep lying about this when people can read it plainly in the abstract.
"On the basis of 688,520 intermediate-frequency, high-quality single nucleotide polymorphisms, we identify several dozen genomic regions that show strong allele frequency differentiation between a pooled sample of five replicate populations selected for accelerated development and pooled controls."
Less than in the fruit-flies of the same "kind"
So what? We have a chromosomal fusion that can account for most of that. Alignment changes doesn't stop them from still having the same genes.
It doesn't matter if the genes go ABCD or ACDB if they are the same genes.
No, this is you making another Tricoplax type error.
That is because this is the actual difference when you look at our genomes. Only 4-6% of our genes are different.
Initial findings are often vague... that is part of being initial... you don't have everything yet and you don't want to sound stupid by jumping the shark.
You should give it a try sometime.
except the 600,000+ single nucleotide changes and dozens of new alleles....
You realize that every individual has between 100 and 200 such mutations in them yeah? That is part of what makes us individuals.:sarcastic
First direct measurement of human genetic mutation rate | Wellcome Trust
Why do you keep lying?
"On the basis of 688,520 intermediate-frequency, high-quality single nucleotide polymorphisms, we identify several dozen genomic regions that show strong allele frequency differentiation between a pooled sample of five replicate populations selected for accelerated development and pooled controls. "
Your "interpretation" is apparently to peddle bald-faced lies and pretend no one will notice.
Just in case you missed it... here it is again:
" On the basis of 688,520 intermediate-frequency, high-quality single nucleotide polymorphisms, we identify several dozen genomic regions that show strong allele frequency differentiation between a pooled sample of five replicate populations selected for accelerated development and pooled controls. "
Interpretation is at least pretending you are using the data given.
wa:do
Last edited:
newhope101
Active Member
"On the basis of 688,520 intermediate-frequency, high-quality single nucleotide polymorphisms, we identify several dozen genomic regions that show strong allele frequency differentiation between a pooled sample of five replicate populations selected for accelerated development and pooled controls."
Generational research on drosophila sheds light on genetic mechanism of evolution
November 1, 2010 by Janet Wilson
Beginning in 2009, Burke ground up Roses fly populations both the live fast and control-group varieties into genetic soups. After computers untangled their long streams of DNA, she pored over all of the flies 14,000 sets of genes, looking for any variations linked to faster development. Burke found not one instance of a single gene spreading quickly. But she isolated more than 500 genes associated with sped-up development.
The experiment, Rose says, is a total vindication of Wright and Fisher and a major defeat for Haldane and a lot of conventional geneticists who have sided with him.
It does not matter about what you are on about. It matters that nothing became fixed in the experiment. That's why a banana is a banana and not a human or a chimp and we share 505 of our genes. That's why a plant has foxp2 but can't talk.
All one needs to do is look to Wiki Genetic drift & Allele to see that allele fixation is part of the process of your evolution by genetic drift or adaptation.
PW Did I hear you assert that allele fixation in populations has nothing to do with evolution? What do you think the difference between species, similar or not, is? I cant work out what you are trying to assert by putting your own spin on the research.
Quite clearly a fruit fly population was unable to fix even 1 advantageous allele over 600 generations in a laboratory setting where it was pressured to, comparable to 12,000 human years. Whether by genetic drift or adaptation the allele did not fix.
Wiki: Fixation (population genetics)
From Wikipedia,
In population genetics, fixation is the change in a gene pool from a situation where there exist at least two variants of a particular gene (allele) to a situation where only one of the alleles remains. The term can refer to a gene in general or particular nucleotide position in the DNA chain (locus).
In the process of substitution a previously non-existent allele arises by mutation and undergoes fixation by spreading through the population by random genetic drift and/or positive selection. Once the frequency of the allele is at 100%, i.e. being the only gene variant present in any member, it is said to be "fixed" in the population.
Similarly, genetic differences between taxa are said to have been fixed in each species
Genetic drift versus natural selection
Although both processes affect evolution, genetic drift operates randomly while natural selection functions non-randomly. While natural selection has a direction, guiding evolution towards heritable adaptations to the current environment, genetic drift has no direction and is guided only by the mathematics of chance.[19] As a result, drift acts upon the genotypic frequencies within a population without regard to their phenotypic effects. In contrast, selection favors the spread of alleles whose phenotypic effects increase survival and/or reproduction of their carriers. Selection lowers the frequencies of alleles that cause unfavorable traits, and ignores those that are neutral.[20]
　
So for the last time I will say; the research showed after 600 generations the allele/s connected to accelerated development, an advantageous allele, did not become fixed in the population. It did not become a part of the difference that may identify a shift towards a new species. For species to become other species and different kinds, and genetically different (and hence be unable to successfully breed), fixation of genes is required. Over a compararice 12,000 human years and 600 fruitfly generations one would expect our researchers would have observed just one that was manipulated into the population. But they didn't.
Generational research on drosophila sheds light on genetic mechanism of evolution
November 1, 2010 by Janet Wilson
Beginning in 2009, Burke ground up Roses fly populations both the live fast and control-group varieties into genetic soups. After computers untangled their long streams of DNA, she pored over all of the flies 14,000 sets of genes, looking for any variations linked to faster development. Burke found not one instance of a single gene spreading quickly. But she isolated more than 500 genes associated with sped-up development.
The experiment, Rose says, is a total vindication of Wright and Fisher and a major defeat for Haldane and a lot of conventional geneticists who have sided with him.
It does not matter about what you are on about. It matters that nothing became fixed in the experiment. That's why a banana is a banana and not a human or a chimp and we share 505 of our genes. That's why a plant has foxp2 but can't talk.
All one needs to do is look to Wiki Genetic drift & Allele to see that allele fixation is part of the process of your evolution by genetic drift or adaptation.
PW Did I hear you assert that allele fixation in populations has nothing to do with evolution? What do you think the difference between species, similar or not, is? I cant work out what you are trying to assert by putting your own spin on the research.
Quite clearly a fruit fly population was unable to fix even 1 advantageous allele over 600 generations in a laboratory setting where it was pressured to, comparable to 12,000 human years. Whether by genetic drift or adaptation the allele did not fix.
Wiki: Fixation (population genetics)
From Wikipedia,
In population genetics, fixation is the change in a gene pool from a situation where there exist at least two variants of a particular gene (allele) to a situation where only one of the alleles remains. The term can refer to a gene in general or particular nucleotide position in the DNA chain (locus).
In the process of substitution a previously non-existent allele arises by mutation and undergoes fixation by spreading through the population by random genetic drift and/or positive selection. Once the frequency of the allele is at 100%, i.e. being the only gene variant present in any member, it is said to be "fixed" in the population.
Similarly, genetic differences between taxa are said to have been fixed in each species
Genetic drift versus natural selection
Although both processes affect evolution, genetic drift operates randomly while natural selection functions non-randomly. While natural selection has a direction, guiding evolution towards heritable adaptations to the current environment, genetic drift has no direction and is guided only by the mathematics of chance.[19] As a result, drift acts upon the genotypic frequencies within a population without regard to their phenotypic effects. In contrast, selection favors the spread of alleles whose phenotypic effects increase survival and/or reproduction of their carriers. Selection lowers the frequencies of alleles that cause unfavorable traits, and ignores those that are neutral.[20]
　
So for the last time I will say; the research showed after 600 generations the allele/s connected to accelerated development, an advantageous allele, did not become fixed in the population. It did not become a part of the difference that may identify a shift towards a new species. For species to become other species and different kinds, and genetically different (and hence be unable to successfully breed), fixation of genes is required. Over a compararice 12,000 human years and 600 fruitfly generations one would expect our researchers would have observed just one that was manipulated into the population. But they didn't.
painted wolf
Grey Muzzle
Do you not understand the difference between "spreading quickly" and "existing".
You claimed repeatedly and falsely that "No genomic change" was found. This is a bald faced lie.
You did not claim "no change spread quickly". I would hope you would honest enough to admit to this mistake... but I have serious doubts given your prior behavior in other similar circumstances.
Why can't you get this simple concept???? :bonk:
There are lots of examples of speciation in fruit flies due to non-polygenic trait mutation.
Diane Dodd's work springs to mind.
Evidence for speciation
I really don't understand why you don't grasp the very simple things I'm trying to explain to you. It's not that difficult.
wa:do
You claimed repeatedly and falsely that "No genomic change" was found. This is a bald faced lie.
You did not claim "no change spread quickly". I would hope you would honest enough to admit to this mistake... but I have serious doubts given your prior behavior in other similar circumstances.
No you didn't... you're making ****e up. Are you really this desperate? :banghead3:
I'm not putting my spin on anything... they clearly say that polygenic traits are difficult if not impossible to fix. That has nothing to do with the fact that single homozygous allele traits fixate easily.
No argument... you are however jumping the shark and reaching a conclusion that is totally antithetical to what the article was about.
FOR THE LAST TIME, THIS ISN'T AN ALLELE! ACCELERATED DEVELOPMENT IS A PHENOTYPE, NOT A GENOTYPE!
Why can't you get this simple concept???? :bonk:
Again, this is showing the difference between polygenic traits and single gene traits. It is much harder for a soft polygenic trait to be fixed in the population... this has been explained several times yet you continue to ignore it.
There are lots of examples of speciation in fruit flies due to non-polygenic trait mutation.
Diane Dodd's work springs to mind.
Evidence for speciation
I really don't understand why you don't grasp the very simple things I'm trying to explain to you. It's not that difficult.
wa:do
