Avida and Genetic Entropy

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101

Sanford’s H1N1 study was factually wrong. The 1917 epidemic grew more virulent in 1918, before attenuating in following years. The following references are from my previous post on another thread, but are pertinent here:

In the 1918–1919 pandemic, a first or spring wave began in March 1918 and spread unevenly through the United States, Europe, and possibly Asia over the next 6 months …Illness rates were high, but death rates in most locales were not appreciably above normal . A second or fall wave spread globally from September to November 1918 and was highly fatal .
Journal of Emerging Infectious Diseases - 1918 Influenza

The 1918 pandemic began with outbreaks of low mortality in the spring and summer, followed by a more lethal wave in the winter .
Vincent Racaniello - Riding the influenza pandemic wave

So much for losing virulence as the pandemic rolls on, due to accumulated mutations. Oh, and this:

Recently the Norwegian Institute of Public Health reported that the mutation , which causes a change from the amino acid aspartic acid to glycine at position 225 of the viral HA protein (D225G), has been identified in 11 of 61 cases (18%) of severe or fatal influenza, but not in any of 205 mild cases .
Vincent Racaniello - The D225G change in 2009 H1N1 influenza virus

I would say that the Sanford paper is a classic correlation failing the demonstration of causation or mechanism, but it’s premise is not even correlated. And that is just getting started with the problems with Sanford’s genetic entropy as applied to epidemiology.

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102

You mean besides the fact life has been on the planet evolving for at least 3.5 billion years and hasn’t all gone extinct? :thinking:

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103

Yes, figure 4 shows recorded empirical reality. Relative fitness is increasing as mutations accumulate in the LTEE. The figure doesn’t show that the mutations accumulating are all deleterious.

So they’re not, in fact, graphing the same thing.

Figure 5 reports the results of a simulation experiment aimed at seeing if the pattern of mutation accumulation observed in figure 4 is consistent with deleterious mutation accumulation. For this simulation, the mutation rate described by Lenski and a biologically realistic Weilbull-type distribution of mutation effects were used. And the thing is that the the observed pattern seen in figure 4 perfectly matches the simulated results of MA, wherein all mutations were deleterious.

All that shows is that if you assume all mutations are deleterious but with extremely small effects invisible to selection, mutations accumulate at roughly the same rate as if they were neutral. But if Sanford had included a curve that showed relative fitness, the mismatch would be completely obvious.

In his simulation, fitness would be declining, while in the real world it’s going up. In other words, in the real world beneficial mutations appear to not only balance out the cumulative fitness loss from deleterious mutations of small effect, but actually outweigh it.

Conclusion: the pattern of mutation accumulation reported in the LTEE experiment is consistent with deleterious mutation accumulation. IOW, with genetic entropy.

We’ve already established many times here that GE is not about deleterious mutations, but about some nebulous information or complexity concept nobody has bothered to define, which will invariably be invoked when real populations show fitness increases rather than decline.

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104

If they’d ignored Sanford’s paper it would have been interpreted to mean it’s because they couldn’t answer it. If they bother to answer, it shows Sanford is hugely important and likely to be right. Heads I win, tails you lose.

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105

No Gil, they don’t match at all because the LTEE obviously did NOT have all deleterious mutations like MA produced. LTEE had mutations which increased fitness. Those are beneficial mutations, not deleterious ones.

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106

I don’t agree with this conclusion. If the world and humanity were 6000 years old we would expect no more than 300000 mutations in the human population based on neutral mutations. Assuming 100 mutations per generation and 20 year generation time.

Isn’t this what the opposing theory is supposed to do?

107

How do you reconcile your opinion that genetic decay is correct with your opinion that lineages can survive for hundreds of millions of years?

108

I don’t know that genetic decay theory is correct. I just don’t think it should be dismissed out of hand. I believe strong purifying selection is playing a role as evidenced by the strong preservation in proteins like alpha actin.

109

It wasn’t dismissed out of hand Bill. It was dismissed because all the scientific evidence shows it is wrong.

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110

No, when you propose a new theory it’s supposed to do a better job of explaining the data.

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111

Here’s what I wrote the last time the subject came up: Suppose there’s a position in our genome that has four possible bases. Two are almost identically good for the organism, two are bad. Suppose it starts out with a bad base there. Millions of years and lots of generations go by. At some point a mutation to one of the good bases occurs and is fixed by natural selection. Thereafter, any mutation at that site to one of the two bad bases will be weeded out by purifying selection and will be rapidly eliminated. So the site will be in one of the two good states. But which one? The difference between them is too small for selection to have an effect, so there is no preference for which occurs. The site can mutate back and forth between them freely.

In order for very slightly deleterious mutations to dominate in sites like this, there has to be some mechanism to get the sequence into the preferred state to start with. What is that mechanism?

That paper has nothing whatever to do with the subject at hand. It’s about mutations that are affected by natural selection.

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112

Bill, your thoughts are incoherent. If species are still around after millions of years, genetic decay is necessarily wrong. And strong purifying selection wouldn’t prevent genetic decay, if there were such a thing; clearly you don’t understand Sanford’s claims.

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113

The so called beneficial mutations you are referring to are only beneficial in a very specific and artificial environment, ie on a glucose diet. But in the real world, these beneficial mutations, which consistently involved loss-of-function, must be seen for what they really are, ie, deleterious mutations that affect total biological functionality, which is the proper way to define fitness.

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114

Says who???

115

You have no idea what you’re talking about. ANY mutation deemed beneficial will only be so WRT the effect it has in a particular environment. There is no such thing as a generic “beneficial” mutation, just as there’s no such thing as a beneficial mutation which reduced reproductive fitness BY DEFINITION.

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116

Sorry, but ‘fitness’ already has a definition in biology. If you want to invent your own concept, give it a new name.

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117

Did you look at the paper I linked above where loss-of-function was reversed, thus gain-of-function?

118

As far as I can tell, Bill, this conjecture is agreed upon by one and only one evolutionary biologist, namely Sanford. The other thousands of evolutionary biologists disagree quite vigorously with the conjecture.

Best,
Chris

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119

Probably most of them are, sure. But that’s going to be true for pretty much any mutation in almost any environment. There is no such thing as unconditionally beneficial mutations that will always be adaptive in any environment. Including the environment E coli normally lives in, in the wild. You change the environment, you alter the conditions that affect whether mutations are beneficial or deleterious.

And this isn’t unusual to E coli of course. The genetic mutations that caused the peppered moths to become darker were beneficial in the context of pollution during the industrial revolution, but when measures were taken to curtail soot and smog, the selective pressure eventually disappeared and the original phenotype became more beneficial again.

People who migrated north to colder climates gradually lost their skin pigmentation which made them able to absorb more UV light for vitamin D synthesis in the skin during the shorter daylight periods of the seasons. If you’re a pale fellow you’re much more likely to get significant sun burns if you move to the African savanna.

And so on and so forth. This really isn’t a difficult concept.

But in the real world

The experiment is part of the real world. The environment might be very simple and artificial, but it is real, and the population is becoming increasingly better adapted to direct competition in it.

these beneficial mutations, which consistently involved loss-of-function

Many of them did. Not all.

must be seen for what they really are, ie, deleterious mutations

No, they’re beneficial. The fitness effect of any given mutation is simply conditional on it’s environment.

that affect total biological functionality, which is the proper way to define fitness.

No it’s entirely wrong and misleading to define it that way. You are erecting a strawman of evolution to knock down when you are insisting mutations must be unconditionally beneficial. It seems extremely odd for you to be talking about the fact that the fitness effect of mutations depend on the environmental context, as if this is evidence against evolution, when this has been understood pretty much since Darwin’s time even though nobody knew about genetic back then.

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120

An increase in death rates is definitely not the same thing as an increase in fitness for the viral agent. For example, Ebola would spread much more widely (and thus be fitter) if its victims didn’t die so quickly.

Best,
Chris

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