That’s a very interesting paper, aquaticus. I think the neutrality of the author comes into immediate question when you see a choice quote like this:
The situation becomes much more absurd and untenable if we assume that the entire genome is functional, as proclaimed by creationists such as Francis Collins, director of the National Institutes of Health
This is the guy who founded BioLogos that he’s talking about, right? And he’s essentially smearing him with the term ‘creationist’…
I infer that the entire logic of his thesis is skewed when I see the following obviously wrong statement:
Finally, we note that in addition to inferring an upper limit on the functional fraction of the human genome, we can also conclude that the fraction of deleterious mutations out of all mutations in functional regions should be very small. If >20% of all mutations in functional regions are deleterious, then the upper limit on the functional fraction of the human genome would be <2%, which is clearly false.
Which is in direct conflict with all sorts of known data as I quoted here:
“Although a few select studies have claimed that a substantial fraction of spontaneous mutations are beneficial under certain conditions (Shaw et al. 2002; Silander et al. 2007;
Dickinson 2008), evidence from diverse sources strongly suggests that the effect of most spontaneous mutations is to reduce fitness (Kibota and Lynch 1996; Keightley and Caballero 1997; Fry et al. 1999; Vassilieva et al. 2000; Wloch et al. 2001; Zeyl and de Visser 2001; Keightley and Lynch 2003;Trindade et al. 2010; Heilbron et al. 2014).”
The moral of the story is that not all mutations are equal. Each additional deleterious mutation sees increased selection to the point that the accumulation of mutations slows down.
This is an oversimplification. Even though most of the genome is nonfunctional, that doesn’t mean mutations in it can’t have fitness effect. It is possible for mutations in nonfunctional DNA to cause it to interfere with important organismal functions that are functional, in a way that negatively affects fitness. And of course, it is also possible for mutations to render a nonfunctional stretch of DNA into a functional one that has a positive effect on fitness, such as when de novo protein coding genes evolve from non-coding DNA.
I’d also take issue with the idea that any mutation is strictly neutral. It may be that a mutation in a nonfunctional piece of DNA has no measurable fitness effect, but does it really have no fitness effect? Given a large enough population, it is conceivable such apparently neutral mutations have extremely weak fitness effects. Exchanging one DNA base for another might cost the addition of a few more carbon and hydrogen atoms, that could have been used on something else, like the synthesis of one more ATP molecule. What is the fitness effect of the loss of one ATP molecule in the context of an entire cell? Probably immeasurably low, and thus effectively invisible to selection in a realistic population. But we couldn’t say it is strictly zero.
@PDPrice, you seem to be suggesting that new strains of the flu virus appear de novo, rather than evolving from prior, existing strains. This is a pretty fantastic claim, and I am fairly sure it is not correct. If this is not what you are taking from the figure you cite, then clarification is needed.
I think we’re going to be friends
You’re being very honest here. I still would not agree with you that most of the genome is nonfunctional, but that’s a debate in and of itself.
If the effect of a mutation is not distinguishable from chance with respect to selection, then I don’t think it really makes a relevant impact. I completely agree with your point, but I think we should err on the side of functional definitions rather than theoretical ones.
That’s what is implied when you say one strain went extinct, and an new strain appeared. If this is not what you mean, then your discussion of the figure, vis-a-vis GE, makes no sense.
Did you know that RNA viruses like this have rather strange behavior of jumping between different kinds of hosts? The Swine Flu post 2009 seems to have been a recombination event from a different host. That means we’re not talking about the Spanish Flu at all post 2009. The Spanish Flu is extinct. The post 2009 H1N1 is a different beast that seems to have gotten some ‘fresh’ (non attenuated) genomic content from swine.
As to viruses, there appears to be at least three big topics that the Genetic Entropy supporters need to address.
Where do “new” viruses come from? It would seem that the emergence of new human pathogens simply come from viruses that used to infect other species. Therefore, these viruses have been around just as long as the 1918 strain of H1N1, and have the same lengthy lineage of ancestors going back in time.
Herd immunity. When people are infected they gain long term immunity through antibodies. Even if a virus increases virulence, it will still be prevented from sweeping through a population as long as there are enough people with long term immunity gained through the adaptive immune system.
Why don’t we see more mutations? The mutation rate is really high in RNA viruses, so we should see many more mutations. The obvious and glaring explanation is negative selection.
??? This is even more confusing. @PDPrice, are you suggesting that the flu viruses routinely incorporate host RNA sequences into one or more of their genomic segments, and that this constitutes something other than an evolutionary progression?
Not in the same way that other organisms do. These recombinations are introducing large amounts of fresh, non-attenuated genetic material and essentially creating a new lineage starting from that point. This is why you can see that the CDC is clearly delineating them as separate lineages.
My understanding could be off, but please enlighten me as to why the CDC is using a completely different color to represent the H1N1 post 2009. Why are they representing it as distinct from the Spanish Flu?
