Do you really understand the mathematics of evolution?

I don't see how that applies here. If there are two possible mutations that confer antibiotic resistance then it would take half as many divisions (on average) to get a antibiotic resistant colony than it would if there was only one possible mutation that confers resistance. Can you please explain why my math is wrong? If we took away competition, what would happen to those mutations you are describing as being fit? Would they be swamped out by the less fit mutations? I think that goes a bit too far. It might be better to say that both DNA evolution and thermodynamics are stochastic processes. It would be helpful if you refrained from insulting peoples' knowledge on the subject and actually addressed what they are saying. Just some advice.I was talking about specific non-coding regions called introns, not non-coding DNA in general. There is non-coding DNA that does have function, but the vast majority of intron sequence shows no evidence of having function. Exons in functioning genes do have function. So what do we see when we compare functioning genes shared by eukaryotic species? We see that sequence conservation in exons is much higher than it is in introns. How do you explain this? How much of that is due to the strength of the selective pressures? That would be dependent on the strength of the selective pressure.

It's the same simplified model we used for calculating 1 mutation. If there is no competition then the less fit variants outnumber the fit variant by billions to one when the mutation occurs. That ratio won't change because there is nothing limiting the growth of the population when there is no competition. Correct. How heat moves through a system is very distantly related to DNA evolution to the point that false analogies start to emerge. Don't be an asshole. Perhaps you are unfamiliar with how exons and introns work. The introns are the pieces of the gene that span the regions between the exons. Introns are clipped out during RNA maturation while the exons are stitched together to produce the mature mRNA. It is the mature mRNA that is translated into protein. The non-coding DNA responsible for regulating gene trascription is found upstream of the first exon in the vast majority of cases. The DNA responsible for post-translational regulation through micro-RNA is found after the last exon. The introns are only very rarely used for gene regulation. If a mutation only confers a tiny increase in fitness it would seem that this allele would increase in number slower than a mutation that is 100% required in order to grow in a specific environment.

Just so we are on the same page, if we use the same simple model that we used before we would need half as many divisions if there are 2 possible mutations for antibiotic resistance as compared to 1 possible mutation for resistance. It is that competition which increases the relative numbers of beneficial mutations. If there is no competition then all mutations are passed on at the same rate. Correct. Thermodynamics is the movement of heat through a system, not the diffusion of alleles. The time it takes to reach sufficient numbers for an additional beneficial mutation to occur in the same lineage is a product of relative fitness.Let's also not forget about sexual reproduction which can combine the beneficial mutations from two lineages.

Any way you slice it, increasing the number of possible beneficial mutations reduces the number of generations needed to get a beneficial mutation. It changes the math as I said earlier. If there is no competition then there are no individuals who are fitter. That doesn't mean that DNA evolution is thermodynamics. That would be the reproduction rate, not absolute fitness. And once again we get insults and condescension. Do you have a point you want to get to, or just insult people while demanding that they do math problems?

Once again, that depends heavily on the number of possible beneficial mutations. If you only need 2 simultaneous mutations out of 2 million possible beneficial sites, then you don't need that many replications, relatively speaking. You can't have detrimental mutations when there is a lack of competition. In a model without competition there are no possible lethal mutations or detrimental mutations. You would also have equal fecundity across all lineages. It is only with competition that you get changes in allele frequencies. That's not thermodynamics. Thermodynamics is the distribution of energy and work in a system. That it happens to share patterns with other processes does not mean the two processes are the same thing. The air pressure from an explosion dissipates by the inverse square law. Photon density decreases from the source by the inverse square law. This doesn't mean that sound waves are photons. Again, why don't you do the math and discuss it? If that is your point then prove it.Let's say there are two dominant beneficial alleles A and B. In the diploid sexually reproducing population you also have the wild type a and b, and the alleles are on separate chromosomes. How many replications does it take to get an individual with AB in the sexually and asexually reproducing populations?Edited by Taq, : No reason given.

Let's see your math. Correct. It seems you are starting to catch on. That would only happen in a model where there is competition. In a model free from competition there would be no lethal mutations. The second law of thermodynamics also pertains to energy. It doesn't pertain to DNA evolution. Just because they use some of the same concepts does not make them the same thing. You seem to be under the impression that Markov chain entropy is the same as thermodynamic entropy. It isn't. Great, then discuss it here. GET TO THE POINT!!

I already knew that. Is that your grand point? This has been common knowledge for a while. Here is an excerpt from TalkOrigins:

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As seen from the phylogeny in Figure 1, the predicted pattern of organisms at any given point in time can be described as "groups within groups", otherwise known as a nested hierarchy. The only known processes that specifically generate unique, nested, hierarchical patterns are branching evolutionary processes. Common descent is a genetic process in which the state of the present generation/individual is dependent only upon genetic changes that have occurred since the most recent ancestral population/individual. Therefore, gradual evolution from common ancestors must conform to the mathematics of Markov processes and Markov chains. Using Markovian mathematics, it can be rigorously proven that branching Markovian replicating systems produce nested hierarchies (Givnish and Sytsma 1997; Harris 1989; Norris 1997). For these reasons, biologists routinely use branching Markov chains to effectively model evolutionary processes, including complex genetic processes, the temporal distributions of surnames in populations (Galton and Watson 1874), and the behavior of pathogens in epidemics.
29+ Evidences for Macroevolution: Part 1

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Thermodynamics deals with energy. A Markov chain model of DNA evolution does not. I want you to discuss them.What point are you trying to make, and how do those papers relate to that point?Edited by Taq, : No reason given.

Could you show us how to properly use mathematics to model human evolution using actual sequences? Thermo = temperature
dynamics = movementAll the laws of thermodynamics involve energy. It's right there in the name. Ok. They use an incorrect model. Now what?

Let's do some back of the envelope calculations. The human mutation rate is about 50 point mutations per person per generation. Let's be conservative and use a 25 year generation time, a constant 100,000 person population, and 5 million years since diverging from chimps. That would be 5 million mutations per generation spread across the entire population. In 5 million years we would have 200,000 generations. 5 million mutations per generation over 200,000 generations is 1E12 mutations that have happened over the history of human evolution.So how many point mutations separate humans and chimps? 35 million. Let's say half of those mutations occurred in each lineage, so 17.5 million mutations in the human lineage. This means that we needed to keep just 0.00175% of the total mutations that did happen.Does that math seem right to you? The energy needed to replicate DNA is a function of its length, not its sequence.Edited by Taq, : No reason given.

You are changing your tune. This is what you said before: That's wrong. As shown above, there were about 1E12 mutations that happened in the human lineage after it split from the chimp lineage. The human haploid genome is only 3E9 bases long. That's enough mutations to change each base 300 times over. Your numbers are way off.Let's look at it a different way. There are 3E9 bases in the human haploid genome, so we would need 9E9 point mutations to get all possible substitutions. At 50 mutations per person, that would be 180 million births to get all mutations. Right now, there are 130 million births each year. It would take less than two years for the current population to get all of those mutations, assuming the chances of all mutations is equal. I am starting to get the feeling that the only things that exist in your universe is the Lenski and Kishony experiments. The energy difference between two DNA sequences is even less. So why do you keep trying to relate DNA sequence to thermodynamics?Edited by Taq, : No reason given.

As I feared, E. coli and the two oft mentioned experiments are all that exists in your universe.You appear to be using the mutation rate from E. coli in human genetics. That is obviously wrong. In E. coli there is just one mutation in every few hundred replications. In humans, there are about 50 mutations in a single replication. You need to account for this.You also need to account for diploid genomes and sexual reproduction. If mutation A happens in one individual and mutation B happens in another individual then their descendants can mate and have offspring with both mutations. Do you agree that it takes less than two years for every possible point mutation to occur in at least one individual within the modern human population? Yes or no? They are only related in the sense that they use some of the same equations.

You seriously have to ask how asexual and sexual reproduction differs mathematically? You once again fail to understand the impact of sexual reproduction. It's a yes or no question.Do you agree that it takes less than two years for every possible point mutation to occur in at least one individual within the modern human population? Yes or no? That number is 0.18E9 for humans. I did the math. Did you look at it? Want to try that one again? Let's use your figure of one mutation per 1E9 bases.E. coli have a 4 million base genome. This means 1 mutation per 250 replications, or 0.004 mutations per replication.Humans have a 6 billion base diploid genome. This means 6 mutations per replication. This also doesn't factor in the fact that the per base mutation rate is higher in humans.

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Through extensive validation, we identified 49 and 35 germline de novo mutations (DNMs) in two trio offspring, as well as 1,586 non-germline DNMs arising either somatically or in the cell-lines from which DNA was derived
https://www.coriell.org/...ationrateswithinhumanfamilies.pdf

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So the human mutation rate is 10 fold higher than in E. coli, which is in keeping with the 50 or so mutations per replication in humans that I keep telling you about.Genome size does affect how many mutations there will be per replication, as does mutation rate. Category error.Edited by Taq, : No reason given.Edited by Taq, : No reason given.

Would you agree that you mutation A and mutation B can occur in different individuals and then be combined in a single descendant? If so, that differs greatly from E. coli, does it not? That 3e9 number is for E. coli, not humans. You keep making this mistake. For humans, you only need 0.18e9 replications. You are ignoring sexual reproduction. The first mutation can happen in one individual and then spread through the population. The second mutation can happen at the same time as the first mutation and spread through the population. Descendants of both lineages can mate and produce offspring with both mutations. With sexual reproduction you can have selection for each mutation in parallel instead of in series.

Lateral genetic transfer occurs between species, not within species. The word you are looking for is "sexual reproduction". I know all about this. I have used this process in the lab to shuttle plasmids between different species of bacteria.What differs greatly is the rate at which this occurs, and it also depends heavily on the strain of E. coli. Many lab strains of E. coli are missing the genes necessary for conjugation. I would suspect that this is the case with the strains used in the the only two experiments that exist in your universe. Then discuss it. Once again, you ignore sexual reproduction. Because HIV is not a diploid eukaryote. That should be obvious to anyone with a tiny inkling of how genetics works. You do it. I don't see any reason to do more math problems for someone who doesn't understand why HIV is not diploid.

Great. Let's see it. I am claiming that HIV is not a diploid organism that reproduces through sexual reproduction. Rare recombination events are nowhere close to mixing two haploid genomes together every generation, as well as about one recombination event per chromosome per generation. It is a question of scale. Because that would require evolution against both herbicides at once. How does this apply to human evolution? Which human adaptations required the same strict selection regime? What is the rate of recombination in HIV?