Peanut Gallery for the debate between mindspawn and RAZD

The back and forth discussion on the earliest life is interesting on its own. RAZD brings up a good point that early life could have had a large genome, but not necessarily a lot of genes (if open reading frames even made sense at that point).Was there any selective pressure for genome size? Perhaps not. Early on, the mere ability to reproduce would have been a massive advantage. It wouldn't be until later that effeciency would be important. This may have allowed an exponential increase in genome sizes after which mutations led to new and novel genes. It is certainly and interesting hypothesis.Edited by Taq, : No reason given.

Edited by bluegenes, 02-04-2013 5:57 AM: negative selection on a grammatical mutationLOL!!

There are various theoretical models of how gene duplications can produce new function, and there's considerable evidence that this can happen in several different ways.One interesting way is the "Escape from Adaptive Conflict" model, known as "EAC". This is based on the fact that some genes perform more than one function. This could hypothetically cause "adaptive conflict", because the ideal allele for one function may not be the same as the ideal for the other. Duplication of such genes, says the theory, could lead to subfunctionalization of each paralog, and to enhanced or new function as each copy of the gene is free to perform only one of the original functions, thus ending the conflict.Here's a recent research paper which presents very good evidence of an example of neofunctionalization arriving in this way. AbstractArticle based on paper

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Abstract

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The evolutionary model escape from adaptive conflict (EAC) posits that adaptive conflict between the old and an emerging new function within a single gene could drive the fixation of gene duplication, where each duplicate can freely optimize one of the functions. Although EAC has been suggested as a common process in functional evolution, definitive cases of neofunctionalization under EAC are lacking, and the molecular mechanisms leading to functional innovation are not well-understood. We report here clear experimental evidence for EAC-driven evolution of type III antifreeze protein gene from an old sialic acid synthase (SAS) gene in an Antarctic zoarcid fish. We found that an SAS gene, having both sialic acid synthase and rudimentary ice-binding activities, became duplicated. In one duplicate, the N-terminal SAS domain was deleted and replaced with a nascent signal peptide, removing pleiotropic structural conflict between SAS and ice-binding functions and allowing rapid optimization of the C-terminal domain to become a secreted protein capable of noncolligative freezing-point depression. This study reveals how minor functionalities in an old gene can be transformed into a distinct survival protein and provides insights into how gene duplicates facing presumed identical selection and mutation pressures at birth could take divergent evolutionary paths.

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Paralogs are identified by sequence similarity. Many paralogs with differing functions have been identified in many different species. Mindspawn faces the daunting task of demonstrating that all of these genes which look like functional coding paralogs are actually not (which is essentially what he is claiming).When something looks like a duck and quacks like a duck, the default is that it's a duck. The onus is not actually on RAZD to show that apparent ducks (or paralogs) are what they appear to be, but on mindspawn to support his extraordinary claim that they are not what they appear to be.Rather him than me!Note the significant added function of the new gene described in the article. "Unlike the SAS enzymes, which remain inside the cell, the AFP III proteins are secreted into the blood or extracellular fluid, where they can more easily disrupt the growth of invading ice crystals."

Interesting. Thanks, bluegenesOne thought I had reading through the thread was that mindspawn is looking at too short a time frame after a duplication.Give the population a few hundred generations, the accumulation of different mutations on the different strands, and presto changeo, totally separate genes with totally different codes and different unique functions.

Yes, or on one copy with the other remaining the same, protected by purifying selection (the classic neofunctionalization without subfunctionalization model). The example in the fish would be rapid subfunctionalization, followed by neofunctionalization in the anti-freeze gene, which ends up producing a protein which is actually secreted into the bloodstream, instead of just performing a mild antifreeze secondary function in the egg cells. The original single gene would have been unlikely to be able to mutate to do the full anti-freeze function of the new gene without damaging its primary function.But there's far more to advantageous duplications than this. Mindspawn is making the argument that was once common amongst creationists, but was applied to all mutations; that they only produce disadvantage and disease. He's applying it to duplications only, as he recognizes that other mutations can cause adaptive advantages.He couldn't be more wrong! Duplications cannot only become advantageous through subsequent mutations, they can be advantageous immediately on arrival. They can increase expression of a protein, which is known to have advantageous effects in some circumstances, as well as disadvantageous and near neutral.For example, a group of primates might have an advantage in increased expression of a protein which helps them digest starch when they are in circumstances in which the readily available food contains a high starch content, but not when they are eating a low starch diet. If different groups of the same species are eating different diets, then different copy numbers of a gene that produced such a protein could be advantageous/disadvantageous/neutral in different groups.And sure enough, there's a wide ranging primate with a variable diet in which that seems to be the case, and selection on copy numbers appears to have acted differently on different groups within the species.Have a skim of this wiki article on copy number variation. Here's the last section, on disease..

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Like other types of genetic variation, some CNVs have been associated with susceptibility or resistance to disease. Gene copy number can be elevated in cancer cells. For instance, the EGFR copy number can be higher than normal in non-small cell lung cancer. In addition, a higher copy number of CCL3L1 has been associated with lower susceptibility to HIV infection, and a low copy number of FCGR3B (the CD16 cell surface immunoglobulin receptor) can increase susceptibility to systemic lupus erythematosus and similar inflammatory autoimmune disorders. Copy number variation has also been associated with autism, schizophrenia, and idiopathic learning disability.

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However, although once touted as the explanation for the elusive hereditary causes of complex diseases like rheumatoid arthritis, the most common CNVs have little or no role in causing disease.

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Among common functional CNVs, gene gains outnumber losses, suggesting that many of them are favored in evolution and, therefore, beneficial in some way. One example of CNV is the human salivary amylase gene (AMY1). This gene is typically present as two diploid copies in chimpanzees. Humans average over 6 copies and may have as many as 15. This is thought to be an adaptation to a high-starch diet that improves the ability to digest starchy foods.

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My bold.AMY1, eh! I like the sound of this AMY. Let's have another date with her in this Nature abstract. Meet Amy againShe's hot!

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Starch consumption is a prominent characteristic of agricultural societies and hunter-gatherers in arid environments. In contrast, rainforest and circum-arctic hunter-gatherers and some pastoralists consume much less starch1, 2, 3. This behavioral variation raises the possibility that different selective pressures have acted on amylase, the enzyme responsible for starch hydrolysis4. We found that copy number of the salivary amylase gene (AMY1) is correlated positively with salivary amylase protein level and that individuals from populations with high-starch diets have, on average, more AMY1 copies than those with traditionally low-starch diets. Comparisons with other loci in a subset of these populations suggest that the extent of AMY1 copy number differentiation is highly unusual. This example of positive selection on a copy number—variable gene is, to our knowledge, one of the first discovered in the human genome. Higher AMY1 copy numbers and protein levels probably improve the digestion of starchy foods and may buffer against the fitness-reducing effects of intestinal disease.

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The importance of all this in relation to the discussion is to show that coding duplications can be advantageous immediately on arrival, and that whether or not they are advantageous can change over time, depending on variable environmental factors.

In Message 52 mindspawn writes:

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Yes, non-coding duplications are occasionally beneficial. This does not contribute towards this thread which is about additional beneficial coding genes.

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Can mindspawn not see the forest for the trees?

I agree with RAZD that it's a good idea for mindspawn to to start a thread on protein coding duplication. For one thing, it gives him a chance to restate his views clearly in the O.P., and, as the O.P. writer, he can direct the subject onto exactly what he wants to discuss.It's also a very interesting subject, regardless of EvC issues, and certainly important in biology.

The Creationists have been able to stave-off the ToE by admitting to the micro-evolution evidence, while saying essentially, that we have no evideence of a macro-evolution that shows the sudden appearance of a brand new organism.Somehow the nectarine and other hybrids have not satisfied them.But recent genetic evidence shows that Act-of-God whereby a mutation joined two ape chromosomes, fusing them to produce the 23 chromosomes found in all humanoids thereafter.This debate and social controversy has ended, and we merely await the slaughter and condescension's of the people who have misread Genesis by getting psychologically set from childhood to protect the teachings of ancient church leader who fail.

The creationists have not "staved-off" the theory of evolution, or any other part of science. They are, in effect, standing in the middle of an 8-lane freeway at rush hour saying, "Go back. You're all going the wrong way."Rather, the history of the last several centuries has shown that creationists have been in constant retreat as one after another of their claims have been shown to be wrong.But they are still trying. (And at least they don't behead those they disagree with! That's sure one way to win an argument!)

Hmmm...The 2 billion Catholics, 2 billion Protestants, and the 1.3 billion muslim are jamming up traffic and absorbing the bumps of the cars pressing them into a circle that still resists the ridicule and arguments against their misconception of Genesis and its meaning.The big question for people like you, for paganism in the West, and the world, in general, is: "What will happen when that one man does come who is embraced by all in that circle, with the power inherent in the mahdi, messiah, or Christ expected to return for just such an ecumenical reason?"Edited by kofh2u, : No reason given.

What is a brand new organism? Am I a brand new organism? I have mutations and a genome sequence that no other human has, so does that make me a brand new organism?This is one of the problems with debating creationists, and why RAZD is being such a stickler with definitions. What creationists try to do, and what mindspawn does throughout the debate, is to require evolution to produce changes that it does not need to produce.For example, RAZD asked:"Let me see if I get this right then: you want a coding gene duplication that suddenly becomes a completely new coding gene that never existed before ... is that correct?"To which mindspawn answered in the affirmative. What mindspawn is doing is saying that new genetic material can only come about through one mechanism, and all other mechanisms will be ignored even if they are observed to happen.Let's use an analogy. I show up at a friends house and he asks me where I parked. I reply that I actually walked since it is only a 30 minute walk from my house to his. His response? Impossible. Either I drove to his house or it had to happen by magic. That is what mindspawn is doing. He is completely ignoring the observed mechanisms that produce increases in genome size because he will only allow it to happen the way mindspawn wants it to happen. Mindspawn is insisting that either I drove to his house or was magically transported there, no other possibilities exist.Kofh2u suffers from the same blinded worldview. Either one species suddenly spawns a completely new species or macro-evolution does not exist. Not once does kofh2u consider that macro-evolution involve descent with modification, not descent into something completely different.

The problem can be illustrated with a simple analogy.Your task is to take 25 dice and throw them in such a way as to get all sixes.There are two ways to do this.The first would be to throw all 25 dice and repeat until you have all sixes. Time to completion: don't wait up!This is what creationists seem to expect. Macro-evolution can't happen until everything is just right, and then presto, a new species!But the second way is to throw the 25 dice and then rethrow only those that are not sixes. Time to completion: you'll be done by tea time easy! This is the way evolution actually occurs, in small increments and building on what has gone before.But creationists inherently deny macro-evolution, so they try to figure the odds that macro-evolution can never happen.They have to! There is no way they can admit just how easy it is, given normal conditions and a long span of time, to have new species evolve.

Hi guysI don’t know whether this is the right place to put this or not, but following the recent stirring of my interest in genetics following the debate, I stumbled across the article Multicellular Life Evolves in Laboratory.I thought it is of interest in this debate.From there I get the following:

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This is actually simple. It doesn’t need mystical complexity or a lot of the things that people have hypothesized special genes, a huge genome, very unnatural conditions, said evolutionary biologist Michael Travisano of the University of Minnesota, co-author of a study Jan. 17 in the Proceedings of the National Academy of Sciences.

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Reading this article, it seems as if no additional complexity (doesn’t matter how the word complexity is defined) is needed in the genomes for the evolution of unicellular organisms to multicellular organisms.It seems as if, for multicellularity to evolve:
1. Increased DNA complexity is not needed and no uniquely functional active coding genes to add fitness are necessary.
2. Genes don't need to duplicate and produce novel functions in the duplicated genes that add fitness.Thus, at least two of the demands from mindspawn in post one of the debate are not needed for the evolution of multicellular organisms. These were: and So, basically, this article says that; for multicellular organisms to evolve from unicellular organisms; all that is necessary would be occurrences such as geographical isolation where a daughter population (or vice versa), experiences different conditions from the original parent population; then multicellularity has been shown to develop with no 'drastic' changes in the genomes.Would my interpretation of that research be correct?Edited by Pressie, : Changed sentenceEdited by Pressie, : Had to rethink second last paragraph

Maybe the article should have been retitled to say: "Darwinism is wrong-life doesn't proceed in complexity through gradual, slow, progressive mutations."But then of course the guy who did the study is a biologist, so that kind of truth is not very pleasant to their ears.

Why would you do that? Nothing in the article says that, nor is that what the authors are claiming.