Petteri_Kiiskinen

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Petteri_Kiiskinen 7 Nov 2007 1:15 UTC
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on: Natural Selection’s Speed Limit and Complexity Bound
Meh, not thinking straight anymore. There are no DNA replications at meiosis, although the recombination does happen here. But still, if there’s no cellular activity during the arrested prophase, the DNA isn’t tested anyway. Now I go to sleep, hoping I wont make any more mistakes.

Petteri_Kiiskinen 7 Nov 2007 1:08 UTC
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on: Natural Selection’s Speed Limit and Complexity Bound
Found factual errors from my previous post, after doing last round of research. Should’ve done it before submitting…

The ova are not in haploid state for the lifetime of the female, but in diploid state, arrested at prophase of meiosis I. Couldn’t find out how much cellular activity they have at this stage, but anyway, there is thus still one DNA replication at only a short period before possible fertilization. This renders much of my above argumentation mostly null. Indeed could be the DNA of ova and spermatozoa isn’t expressed at all at the haploid cell. This would leave the pre-birth selection pressure only to spontaneous zygote abortions (which have other explanations than mere point mutations to them as well).

Petteri_Kiiskinen 7 Nov 2007 0:37 UTC
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on: Natural Selection’s Speed Limit and Complexity Bound
Eliezer, I have to admit I’m not studied on the field enough, and I’ve not read papers on this particular. The initial cell bodies of a gamete of course come from the parent cell.

However after that, they have to keep on living. And they do this using their own genetic material to support and repair themselves, manufacturing new cell bodies, enzymes and other constituting proteins as old bodies deterioriate. All ovum in ovaries are present at birth of the female, thus having to be able to maintain their function at least up to menopause. This makes them one of the longest living cells beside neurons, while being haploid at that. Of course, as far as protein synthesis goes, I dont think this feat requires the usage of that great percentage of all genes after all, but it’s something anyway.

On the other hand, in the germ line there is a development phase from a fertilized ovum to the new gonads, where the germ line DNA is carried across multiple divisions in singular line. This accumulates more of said mutations, while selecting only against the most destructive mutations which express themselves in a relatively short period of time (the germ line cells are stem cells up to when gonad cells start to actually differentiate, and the differentiation obviously begins from more or less healthy stem cells at that point). Still, on the whole, this increases the corruptive pressure.

However, what I find more interesting, is how the point mutations affect regulatory areas and relevant ‘junk’ DNA. But we just don’t know enough of the mechanics there.

This is my relevant contribution.

Other commenters have made interesting points on how small adverse effect mutations dont really spread out quickly in the population, and how when selection actually happens post birth, it often tends to be the result of a combined work of many such adverse mutations, not just one. In this case, one death removes, on the average, more than just one adverse mutation from the pool. I haven’t delved deeper into the subject so I can’t say if this contradicts the initial assumption of “one mutation, one death” or not, although to me it seems it does. Why wouldn’t it? My apologies if this is ignorant question, I would do the maths now myself, but it’s late and I need the sleep.

Petteri_Kiiskinen 6 Nov 2007 13:38 UTC
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on: Natural Selection’s Speed Limit and Complexity Bound
A point to note is that corrupting pressure to genome through adverse point mutations occurring on protein coding DNA regions are partly counterbalanced by selection happening already before birth, in form of miscarriages (late and early) and cell death or cell inefficiency during earlier stages of the germline development, even before fertilization.

Even if the value of 1 bit per generation holds true for addition of new ‘relevant’ information, the above acts as additional positive factor that only acts to negate the degrading effects of random mutations. Obviously this doesn’t matter when talking about post-birth (meaning, say, post-one-week-after-inception, assuming only a lowly value of 50% of miscarrying after that point) relevant DNA information, which thus might still be capped around 25MB. However, it’s far from obvious how and where exactly this information is embedded in the DNA.

It would seem that more relevant than protein data itself is the data that affects how and in which situations proteins express. This hints that post-birth relevant information is stored elsewhere, in regulating sections and perhaps in the ‘junk’ DNA regions. And what comes to understanding these regions, our knowledge is flimsy. The information might actually be encoded in these regions in a manner that allows for error-correction schemes not quite unlike the Von Neumann point made earlier in the comments, about computer memory error correction.

I think it’s not fitting to state that post-birth relevant information is “the meaningful DNA specifying a human”, without stretching the meaning. After all, what good is a program without understanding the interpreter and having a platform to run it on?

To sum up: Adverse point mutation pressure occuring in protein coding regions is at least partially offset in early stages of germ line, where the quantities selected upon are huge. Point mutations occuring in other regions have implications and mechanisms which are not nearly well enough understood. Thus I dont see a solid ground for the quantitative conclusions made in this article, and only some ground for the qualitative conclusions.