Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."

The vast majority of junk DNA is defective transposons, so we understand they are junk because we do know what they are. We also know what introns are. Only about 10% of the human genome is of unknown origin. You can get a rundown at Sandwalk: Sandwalk: What's In Your Genome? - The Pie Chart There is also the C paradox where very similar organisms differ greatly in their genome size. This is where the Onion test comes from because different onion species can differ by billions of bases.Moran also has a good list for topics you will need to address if you want to wade into the junk DNA discussion:

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1. Genetic Load
Every newborn human baby has about 100 mutations not found in either parent. If most of our genome contained functional sequence information, then this would be an intolerable genetic load. Only a small percentage of our genome can contain important sequence information suggesting strongly that most of our genome is junk.

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2. C-Value Paradox
A comparison of genomes from closely related species shows that genome size can vary by a factor of ten or more. The only reasonable explanation is that most of the DNA in the larger genomes is junk.

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3. Modern Evolutionary Theory
Nothing in biology makes sense except in the light of population genetics. The modern understanding of evolution is perfectly consistent with the presence of large amounts of junk DNA in a genome.

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4. Pseudogenes and broken genes are junk
More than half of our genomes consists of pseudogenes, including broken transposons and bits and pieces of transposons. A few may have secondarily acquired a function but, to a first approximation, broken genes are junk.

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5. Most of the genome is not conserved
Most of the DNA sequences in large genomes is not conserved. These sequences diverge at a rate consistent with fixation of neutral alleles by random genetic drift. This strongly suggests that it does not have a function although one can't rule out some unknown function that doesn't depend on sequence.
Sandwalk: Five Things You Should Know if You Want to Participate in the Junk DNA Debate

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Humans and chimps share beneficial alleles that were found in their common ancestor. Humans and chimps also have different beneficial alleles that cause them to be different from each other. This isn't rocket science. Because evolution is a contingent process, and the contingency in this example is the genetic background of the starting species. The chimp lineage has added 5 million years of mutations to the genome of the common ancestor, so it is no longer a valid starting point to "repeat" human evolution. It's the same explanation you are using. I have no disagreements that there is clonal interference in those two experiments, nor do I disagree with your general description of those experiments. There may be some disagreements in the specifics, but those are irrelevant to the larger discussions. What I disagree with is the application of those observations to sexually reproducing populations.How many times do I have to explain this? Your explanation is based on false assumptions.

Yes, it does.

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To investigate how sex improves the efficiency of selection, we analyzed the dynamics of adaptation. As in earlier studies21,22, asexual populations exhibit signatures of hitchhiking and clonal interference (Figure 2a–d). Groups of functionally unrelated mutations, linked within the same genetic background, change in frequency together as clonal cohorts. The outcomes of evolution are determined by competition between these cohorts. In contrast, sexual populations are not characterized by cohorts of linked mutations (Figure 2e–h). Instead, the dynamics of each mutation is largely independent of other variation in the population. In these populations, mutations that occur on different backgrounds fix independently, while others briefly hitchhike to moderate frequencies where they persist or are eliminated from the population.
Sex Speeds Adaptation by Altering the Dynamics of Molecular Evolution - PMC

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In sexual populations, the alleles that confer effective use of limited resources are put into the same genetic background so that they don't compete with one another. The frequency of a beneficial allele in sexually reproducing populations is independent of other alleles.

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Instead, the dynamics of each mutation is largely independent of other variation in the population. In these populations, mutations that occur on different backgrounds fix independently, while others briefly hitchhike to moderate frequencies where they persist or are eliminated from the population.
Sex Speeds Adaptation by Altering the Dynamics of Molecular Evolution - PMC

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What you can't seem to understand is that the genetic outcome of this process is different in asexual and sexual populations.

The only examples of clonal interference you have given me are in asexual populations.You have also not given me any physics that disproves the observation of beneficial mutations fixing independently in sexually reproducing populations, as seen in the Desai experiment. If you claim that physics requires clonal interference in sexual populations but no clonal interference is seen, then it is your understanding of physics that is wrong, not reality. In the Desai experiment the beneficial mutations are put into the same genetic background so that they no longer compete with one another. That's the explanation.

Are we talking about this paper?https://www.desai-lab.com/...ostamcdonaldnguyenbadesai21.pdfIf so, then you are referring to asexual populations. There were no sexually reproducing populations in that paper. All of the populations were asexual.

If you look at the actual title it doesn't have the "(with asexual reproduction and sexual reproduction)" part. You added that. There were no sexually reproducing populations in the paper. Both the diploid and haploid populations were reproducing asexually. This is why the authors stated:"Our experiment provides an opportunity to compare asexual adaptation in diploids to that in haploids, and to characterize diploid-specific aspects of the evolutionary dynamics (Figure 8). "All populations were asexual. ALL. However, the genetic outcome of that competition will be different in asexual and sexual populations. In asexual populations competition is between whole genomes because there is no recombination. In sexual populations, competition is between alleles within the same gene, not between genes and not between whole genomes. For this reason, beneficial mutations at different loci can increase in frequency together. Beneficial mutations at different loci do not compete with one another in the case of sexual reproduction.

I'm looking at the right paper. It specifically states that the diploid populations were reproducing asexually, as were the haploid populations. All of the populations in that paper were reproducing asexually. ALL."Our experiment provides an opportunity to compare asexual adaptation in diploids to that in haploids, and to characterize diploid-specific aspects of the evolutionary dynamics (Figure 8). "That's in the middle of pg. 11.

There were no sexually reproducing yeast in that paper. The diploid population was reproducing asexually, and the haploid populations were either MATa or MATa(alpha) only which means they were incapable of mating and could only reproduce asexually. In order to have mating between haploid cells you need different mating types, but the different mating types were never in the same culture. The haploid cells were also mating type stable due to the mutations introduced by Desai et al.The title says nothing about sexually reproducing yeast. The paper says nothing about sexually reproducing populations in the paper. You added that part in. I suspect you saw "diploid" and assumed it was sexual reproduction. It isn't.From the Desai 2021 paper:"Our experiment provides an opportunity to compare asexual adaptation in diploids to that in haploids, and to characterize diploid-specific aspects of the evolutionary dynamics (Figure 8). " I fully accept that biological organisms are competing for limited resources. It's not that tough to understand.Is my explanation of beneficial traits moving into the same genetic background too complicated for you to understand?

This page has a good explanation for the life cycle in brewer's yeast.What is Yeast? - Singer InstrumentsBrewer's yeast can reproduce asexually as either a haploid cell (one copy of genome) or a diploid cell (two copies of genome, like in humans).Haploid can reproduce asexually (budding) if they don't conjugate with other haploid cells. Haploid cells will only conjugate (i.e. play Barry White) if they are opposite "sexes" called MATa and MATalpha. Two MATa's can't conjugate, and neither can two MATalpha's.Once the haploid cells conjugate you get a diploid cell which can continue to reproduce asexually through budding. However, if the diploid cells experience stress in the environment they can sporulate which produces the haploid cells with opposite sexes. That starts the haploid growth phase, rinse and repeat.So if you see a paper describing budding diploid cells this does not mean that they are sexually reproducing. Diploid budding yeast can and do reproduce asexually, just as the somatic diploid cells in your own body reproduce asexually. If an experiment does have a sexual cycle then you will see it described in the Methods section where diploid cells are forced to sporulate under specific conditions, and then there is either selection for diploids or haploids afterwards. If it simply describes the growth of diploid budding yeast with the same conditions throughout then it is asexually reproducing diploid yeast.Hope that clears up any confusion.

What does change is the genetic outcome of that competition. That doesn't change the fact that clonal interference does not occur in sexually reproducing populations. I think we all agree that there are conditions where neither asexually or sexually reproducing populations can not overcome environmental challenges, but that doesn't give you the right to misrepresent the underlying genetic changes. I did search the literature, and I found the Desai paper which describes how sexual reproduction allowed the population in the experiment to avoid clonal interference. Are you saying that the populations in Desai's experiment violated the first law of thermodynamics? Sexual reproduction does reduce the number of deleterious and neutral mutations that fix in the population. However, sexual reproduction is far more efficient at driving beneficial alleles towards fixation as shown in the Desai experiment. That has zero to do with either asexual or sexual reproduction. The situation you ignore is where one field uses herbicide A and another field uses herbicide B. You could get resistance that occurs in either field. If those two phenotypes mate then you get offspring that are resistant to both herbicides. I have that experiment.Sex speeds adaptation by altering the dynamics of molecular evolution | Nature

I'm an atheist and I will gladly admit that I don't know how life started. Perhaps you should ask what atheists think instead of erecting strawmen. What isn't adequate about Darwinian theory?

Yep. The peak of Mt. Stupid in the Dunning-Kruger effect.

Funny how you can't quote any of them actually saying that. You can continue to beat up your strawmen, or you can actually engage with what we are actually saying.

I have a paper with an experiment that demonstrates sexual reproduction overcomes clonal interference.

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To investigate how sex improves the efficiency of selection, we analysed the dynamics of adaptation. As in earlier studies21,22, asexual populations exhibit signatures of hitchhiking and clonal interference (Fig. 2a–d). Groups of functionally unrelated mutations, linked within the same genetic background, change in frequency together as clonal cohorts. The outcomes of evolution are determined by competition between these cohorts. In contrast, sexual populations are not characterized by cohorts of linked mutations (Fig. 2e–h). Instead, the dynamics of each mutation is largely independent of other variation in the population. In these populations, mutations that occur on different backgrounds fix independently, while others briefly hitchhike to moderate frequencies where they persist or are eliminated from the population.
Sex speeds adaptation by altering the dynamics of molecular evolution | Nature

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I can do one better. I can cite an experiment where this very thing was done. See above.I can also cite this paper which used computer simulation to model asexual and sexual reproduction: Sex solves Haldane’s dilemmaPay careful attention to Fig 2 where sexual reproduction overcomes clonal interference in the computer simulation. A quote from the paper:

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The strategy used by nature is somewhat analogous to the process of parallel computing. Since recombination decouples the allelic changes at a given locus from changes at other loci, it effectively decomposes multi-locus selection into several simultaneous instances of individual selection.

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So I have both a real world experiment and a computer simulation demonstrating exactly what I have been claiming all along.

What do you mean "improve the probability of an adaptive recombination event"?In the conditions where sexual reproduction alleviates clonal interference, is there a violation of the first law of thermodynamics?