Summations Only

Can you point to any step in the evolution of feathers that required 2 simultaneous mutations? If not, WHAT ARE YOU GOING ON ABOUT???????

And this is a problem how? I am still waiting for you to explain how this is a problem for rmns.

Then please use that model on vertebrate genomes and show us which genetic differences between species could not be produced by rmns. If you can't do that, THEN WHAT ARE YOU GOING ON ABOUT?

We have plenty of living species whose genomes we can compare. For example, we have chimps and humans. When we use mutation rate, population size, and generation time to calculate the divergence time for genetic data you get 5-8 million years which matches the hominid fossil record.

Can you name a single beneficial difference between any two vertebrate species that required 5 simultaneous mutations? If not, THEN WHAT ARE YOU GOING ON ABOUT??????

In an attempt to communicate your's, mine, and other's confusion over the argument being made by Kleinman in this thread, I will attempt to configure the argument in terms of the lottery. It is at this point that we all just scratch our heads and wonder what in the world he is arguing against.Edited by Taq, : No reason given.Edited by Taq, : No reason given.

The problem is that the bacterial examples you use show that RMNS can produce the observed evolution of adaptations in those bacteria. You have yet to show a real example in a real species where RMNS can not produce the observed differences between two species or a species and its ancestors. You claim that RMNS can not produce the differences we do see, but you have yet to show us a single example where this is true. You need to describe why the physics and mathematics of RMNS disqualifies RMNS as the mechanism behind the divergence of species with reference to specific genetic differences.

When will be getting to real replicators and real genomes?

They accumulate through selection, so I don't see how the mathematics of random recombination are applicable. The non-random rates of survival and reproduction seem to be more applicable in this instance.

The main problem with your HIV example is that the beneficial mutations are not additive. In most situations, beneficial mutations are additive.What I mean by additive is if A and B are both beneficial mutations on their own, then an individual with both A and B will be more fit than individuals with just A or B. In the case of multi-drug treatment and HIV, there is no way for an amplification of just A or just B because the individual viruses with just one potentially beneficially mutation do not reproduce at a higher rate.We could use an example in humans to show why your HIV example doesn't work. In humans, there has been selection for both malaria resistance and melanin production. Individuals with either darker skin or resistance to malaria will do better than individuals without either trait in lower latitudes that experience endemic rates of malaria. Both traits will be selected for independently. Individuals who receive both traits will be even fitter than individuals with just one of those traits.As we can see, your HIV model fails to model real life, both because it lacks additive fitness and it lacks sexual recombination. In human populations, you don't have to wait for dark skin to become fixed before malaria resistance can be selected for. Both can be selected for in individual lineages, and through sexual recombination you can have individuals inherit both beneficial mutations.Edited by Taq, : No reason given.

I don't have a reference at hand, but I may find time to find one.I think my example of melanin production and malaria resistance should suffice, unless someone can explain how darker skin will not be selected for unless someone also has mutations that confer malarial resistance (and visa versa).

Then let's see your math with specific examples in real genomes.

I don't see how that addresses anything in my post.Let's use military tanks as an example. Let's say that two possible upgrades for a tank are thicker armor and a more powerful main gun. A tank with either thicker armor or a more powerful gun would be better. A tank with BOTH thicker armor and a more powerful gun would be better than a tank with just one upgrade. The upgrades are additive in that both upgrades add up to a better tank than a single upgrade by itself.This is often how beneficial mutations work. A beneficial mutation is beneficial all by itself. When it is combined with another beneficial mutation, the individual with two beneficial mutations is more fit than an individual with just one of those beneficial mutations.The problem with your HIV model is that it doesn't take this into account. You are only looking at situations where you need both mutations in order to see an increase in fitness. As discussed earlier, this isn't always the case in the real world.Edited by Taq, : No reason given.

Recombination events are random mutations, and recombination events can produce new alleles.

Sorry for the confusion.With multidrug therapy, if a virus gains a mutation that confers resistance to just one of the drugs it will not be fitter than other viruses without that same mutation. This means that individual viral particles with just one mutation to one drug will replicate at the same rate as those without the mutation.