That’s correct. I’m not interested in substantive dialogue with someone who is ignorant of the topic and unwilling to accept correction. Sorry if that’s rude of me, but I have actual scientific work to do.
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Yes, it was rude of you. Your comments are unhelpful, and your claim that I’m ignorant of the topic is unfounded. Especially given that I’m one of the only people involved here that has actually read Dr Sanford’s book that we’re supposed to be debating.
If you read my previous comments, you would have figured out in what sense GE is “found wanting” with regards to data.
For the sake of clarity. You have claimed that the bulk of nearly-neutral mutations are slightly deleterious. You have been asked to support this with data, but you haven’t. That is what I meant by data finding GE wanting, since the accumulation of SDMs invisible to natural selection over generations is crucial to the GE argument.
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You empirically demonstrated your ignorance on the topic. The fact you’ve run from so much data shows the level of your intellectual cowardice. All you do is grandstand and preach.
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Everyone note Paul dodged these critical questions too. What a surprise.
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The topic I am referring to is population genetics. The last time (I think) that I tried to engage with you on population genetics, it was with this exchange on neutral theory:
This was followed by crickets from you. Feel free to correct your misstatement now to demonstrate your intellectual honesty, but again I’m not interested in a dialogue.
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You would sound more convincing if you actually provided some data yourself.
If you want the rest of us to read it, you need to convince us that it’s worth reading first.
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I don’t see any evidence that you’ve examined the data, so your saying anything about “All the data we have available…” is not credible.
Not when it is packaged in virions.
They do, but not because RNA is unstable. It’s because RNA replicases are more error-prone.
You’re obviously not here for dialogue. You’re here to debate and then run. Dialogue and debate are not synonyms, just as subtypes and strains and classes are not synonyms when discussing influenza viruses.
Have you contacted the CDC about their error in making vaccines against H1N1, when according to you it is extinct?
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We’re debating a hypothesis, not a book.
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I appreciate even the slightest hint of chivalry on this forum so thank you to you and @PDPrice in this thread (although @Dan_Eastwood earns highest points in this regard in the forum)
But don’t worry - I pay LOTS of attention to behavior. I notice when either side may overstate their case or be too dismissive. You can just call me an ultracrepidarian (just discovered this word 
) but at the same time I may have a knack for seeing holes in arguments as well as contractions. There are no perfect scientists.
Interesting that their population size is so large they would accumulate more mutations, therefore the worst deleterious mutations would have a chance to be selected against. And since we know they have more mutations it would seem the empirical evidence fits GE.
Haven’t some animals lost their y chromosome?
Perhaps God created resiliency and redundancy in the system.
This is possibly a fair criticism I think @PDPrice or maybe not and I wonder if Carter or Sanford could attempt it. If you give an inch they will take a mile. Sanford has basically retired it appears to me, but GE will still live on and needs to be sharpened and refined for future generations until current theory has died. I think it will because the genetic data will continue to accumulate and show it doesn’t work. But I would like to see a paper on what research has been done on natural reservoirs. It seems there’s a lot we don’t know, but that should be exposed IMO to weaken their arguments against GE.
But also @CrisprCAS9 you’re the one who said this.
Thanks for sharing that paper because apparently there’s also a lot you don’t know about adaptive evolution. So I don’t think you and other scientists should be so dismissive of alternative theories.
we are still largely ignorant as to how, exactly, natural selection acting on beneficial mutations leads to adaptation (Orr 2005). There are many fundamental questions that remain largely unanswered, including: Where do most adaptive genetic variants come from—ancestral variation or de novo mutation? How strong is selection, on average, and does its strength vary for different types of phenotypic traits? Does the strength of selection change in a predictable way as mutations are fixed and populations approach phenotypic optima? Do most adaptations involve a small number of genes with large phenotypic effects or many genes of small effect? To what extent do competing ecological demands, genetic linkage, and pleiotropy constrain adaptation? Finally, how often does natural selection rely on the same genes and/or mutations to drive convergent evolution? Answering these questions is challenging because it requires knowing the precise phenotypic targets of selection, identifying the genetic loci contributing to those adaptive traits, and measuring the strength of selection acting on both phenotypes and genotypes.
As modeled by GE, larger population sizes reduce the rate of accumulation.
So plenty of time on his hands, then.
Yes, I did say that. And I stand by it. But you will hopefully recognize the difference between saying ‘here are a few models and equations, with the following limitations and assumptions, being applicable in the following circumstances and sorts of populations’ and saying ‘We’ve got this model, it works! Trust us! But don’t ask for math, because biology is too complicated!’.
Sure, definitely. All models are wrong, some models are useful. There are many areas that still need work. That doesn’t imply that the broader theory is invalid. Further, if you look at the things the authors mention, evolution works under all extents of all of the outstanding questions.
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You ignored my earlier question. GE claims VDMs accumulate because they are invisible to selection. Now you say they are selected against in mice but not humans. Do you want to think about what you are saying and come up with one coherent story?
Sorry dear but GE “theory” was dead on arrival.
What in the world does that have to do with GE?
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You do not, just so you know.
No, that’s not how it works. The worst deleterious mutations are selected against regardless of population size. A large population just decreases the range of what slightly deleterious mutations can’t be selected against, thus decreasing the amount of GE. Having more mutations (which mice do, per year though not per generation) increases the amount of GE.
Not to my knowledge. Some animals don’t have Y chromosomes, but I doubt it’s clear whether their ancestors had them. At any rate, this has zero to do with GE.
If so, there is no GE. Or are you claiming that mice have this resilience but humans lack it?
What future generations? Aren’t we all doomed to extinction quite soon?
There are no “natural reservoirs” in the sense Sanford means, places where viruses can hang out without accumulating mutations. So there can be no research on them.
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My understanding is that in GE the number of mutations available for selection increases as generation time decreases AND population size increases.
Maybe that’s counterintuitive but it makes sense to me. Since natural selection is differential reproduction, the probability for variance in fitness increases with population size and low generation time, so then natural selection is more efficient.
So I do think you are understanding it wrong, if I am correct on that. I’m still learning, so I’m not going to guarantee I’m understanding it right by any means. 
When there is no variance in fitness in a small population and deleterious mutations accumulate, that’s what leads to mutation meltdown and extinction, correct?
It fits with special creation of organisms. The y-chromosome didn’t evolve into existence. It was created and is accumulating harmful mutations.
But as soon as the Y chromosome existed, it was primed to shrink. Over time, genes develop mutations, many of which are harmful, Wilson said.
Loss of the Y chromosome isn’t off the table — it’s happened to other species, Graves pointed out. Two species of underground rodents called mole voles have independently lost their Y chromosomes. So have three endangered species of spiny rats living on several small islands in Japan.
Is the Y chromosome dying out? | Live Science
Men are at a higher risk of developing and dying of sex-nonspecific cancers, but the reasons for this remains unknown. Y chromosome loss and rearrangements have been associated with different types of cancer, such as bladder cancer, male sex cord stromal tumors, lung cancer and esophageal carcinoma33,37. Loss of Y chromosome has been found in association with smoking, shorter survival and a higher risk of cancer (urothelial bladder cancer, pancreatic cancer, esophageal carcinoma, head and neck carcinoma, renal cell carcinoma and in cancer cell lines of hepatocellular carcinoma). It was suggested that LOY (loss of Y chromosome) in blood cells could become a predictive biomarker of male carcinogenesis39, because it is known that the Y chromosome is frequently lost in hematopoietic cells, representing the most common somatic alteration in men and it has a demonstrated role in cancer susceptibility40. So a better knowledge of more Y chromosome sequences will help us develop a deeper understanding between Y chromosome alterations and male cancer development.
https://www.nature.com/articles/s41598-018-27819-x
Sure.
I guess I’ll have to try harder to prove it. I did kinda mess up your reliance on Euthyphro’s Dilemma though, huh? Sorry about that.
Larger effective population sizes lower the threshold for efficient selection, lowering the rate of deleterious mutation accumulation and increasing the rate of beneficial mutation accumulation.
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What is your justification for that understanding?
If. Do you think it possible that you are not correct and you’re the one who is understanding it wrong. After all, you have come to your studies quite recently, unlike the various actual biologists posting here. Your understanding, as it happens, is wrong.
You understand that some groups have Y chromosomes, some have W chromosomes, some have autosomal alleles, some have only dosage of X chromosomes, and some have only environmental factors (temperature, mainly) to determine sex. X and Y chromosomes have evolved many times from autosomes. (XY is just the name given to sex determination systems in which the male is heterozygous. ZW is the name given to systems in which the female is heterozygous.) Don’t confuse your ignorance of biology with evidence.
You will note that the loss of Y chromosomes in the examples you give didn’t harm the species. And you will note that the cancers develop not from loss of Y chromosomes in individuals but in somatic cell lines, nothing like what you’re talking about or relevant to the discussion.
Your cheerful arrogance does you no credit. I’m not sure what triumph you’re talking about here, but it’s definitely imaginary.
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Show me this research for selection for simple organisms.
Reading their literature. That’s the takeaway I’m getting.
I meant they might be understanding GE wrong, in regards to selection. It’s new to everyone.
Begging the question.
Either I’m confused or you’re ignoring what I quoted in the paper. But either way, I can google to provide more evidence.
The idea to study the Y chromosome came about thanks to a discovery from Dr. Kantoff’s lab that was reported in July 2018 in the Journal of Clinical Investigation. While studying prostate cancer, his team found that a gene on the Y chromosome called KDM5D determines whether prostate cancer will respond to the chemotherapy drug docetaxel (Taxotere®). Additionally, mutations in the gene in prostate cancer cells were associated with poor overall prognosis.
“I was fascinated when I heard about this project,” says MSK computational biologist Nikolaus Schultz, who is spearheading the data analysis portion of the research. “When we look at tumor samples, the mutations that are reported are for the autosomes and usually the X chromosome. Most of the Y chromosome is unexplored, even though researchers have been focused on cancer genomics for more than ten years.”
You are very confused.
What people say is not evidence. Moreover, they are talking about cancer’s origin in somatic cells, as John noted.
Please stop pretending that you are dealing with evidence when you are only dealing (very poorly) with words. There’s a difference.
There’s a reason why you stay far away from evidence.
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It is the foundation of nearly neutral theory, which Sanford uses as the core of GE.
I’ve been talking about GE for several years now. It isn’t new to everyone.
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No, GE is not new to everyone. Here are excerpts from an email I sent to Sanford in 2009. (I don’t have the full, original email, just the parts he quoted in responding to me). I have known about Sanford’s model for a long time, and I think the email contents show that I did not dismiss it without thinking about it at some length,
[The following expands on point 2 above. ‘Soft selection’ is selection that affects only relative fitness, not absolute fitness.]
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