REAL NS is a problem for common descent, fitness peaks, in Eukaryotic evolution

Darwin’s vision of what he mistakenly calls natural selection might be more rightly characterized an imagined or fantasized version of selection, not what really happens and nature.

Thus his theory of “Natural Selection” is an equivocation, where his word “Natural” isn’t really what happens in nature, but rather how he and subsequent evolutionary biologists have imagined what happens in nature.

Darwin said:

It may be said that natural selection is daily and hourly scrutinizing throughout the world, every variation, even the slightest; rejecting that which is bad, preserving and adding up all that is good; silently and insensibly working, whenever and wherever opportunity offers, at the improvement of each organic being in relation to its organic and inorganic conditions of life.

Quoted also in:

The Death of Natural Selection - Scientific American Blog Network

But selection doesn’t improve each organic being when it sends them to extinction, and selection often selects for damage, not for improvement as in numerous cases of reductive evolution, and Behe would rightly argue DE-volution is more the natural norm than the exception.

But beyond that, natural selection would be in impediment to evolution of complexity in many cases. Complexity as in more integrated systems. And Darwin somewhat understood the problem of extravagance and rube goldberg complexity when he quipped that the Peacock’s tail made him sick.

The problem of NS preventing evolution emerges in numerous places in the evolution of Eukaryotes. For example consider these prokaryotic and eukaryotic system from textbook biochemistry:

vs.

eukaryote_protein_synthesis_initiation1%5B1%5D

Granted the eukaryote might not necessarily evolve from exactly the system depicted for the present-day prokaryote, but whatever the ancestor looked like, it would pose comparable problems to hypothetically evolving a prokaryote to the eukaryote.

Because there are several proteins involved, there are thousands of ways to break the prokaryotic system, but even a few would immediately be lethal (and thus selected against). Consider the IF-3 connect to the E and the IF-1 connecting to in the 30S subunit. That is the reverse situation in the corresponding Eukaryotic system. There is no gradual path to this, and it has to work instantly and adequately, otherwise the system dies. And there are numerous other problems as there are so many more complexes involved in the Eukaryotic cycle that have to pop in and be functional from the start.

Natural selection would preclude such evolution, and the evidence of this is, ironically the supposed conservation of the Prokaryotic architecture over hundreds of millions of years. I mean, one should not be saying, “selection conserves this feature” and then simultaneously arguing selection evolved away from this feature! That is a logical contradiction.

Selection preventing evolution by constraining or “conserving” an architecture is related to the problem of fitness peaks in evolutionary algorithms. Now someone could say “fitness landscapes change”, but those claims are unjustified in light of mechanical considerations of life critical systems such as those above, not to mention it is inconsistent with insisting something is “conserved” for hundreds of millions, if not billions of years.

I will post a few other examples of things that caught my eye. I won’t immediately say the differing operation of helicases is un-evolvable, but still this gives me pause:

helicases

From:

This is a picture I may show in an upcoming presentation. Part of the presentation is why common descent would require miracles to make it feasible

Double stranded break repair exists (I presume) in prokaryotes.

But look at one example of how this is done in the context of Eukaryotic chromatin that must involve histones as a matter of principle. Boggles the mind. Failure to manage doubles stranded breaks is lethal to a cell and/or cell lineage:

From:

https://clincancerres.aacrjournals.org/content/16/18/4543

Model of histone modifications and chromatin remodeling during DNA DSB repair, step 1: Recognition and signaling of a DSB. γ-H2AX plays a key role in DNA damage signaling, acting as a platform of assembly for the repair factors as well as for checkpoint proteins. Immediately following the apparition of a DSB, the MRN complex binds DNA ends and participates in ATM kinase recruitment. ATM then rapidly phosphorylates the H2AX histone variant at the site of the break. Phospho-H2AX, also called γ-H2AX, allows the binding, retention, and accumulation at the break of the complexes involved in the DDR. The simultaneous presence of the RSC remodeling complex at the break may facilitate the access of the recruited repair factors. Indeed, the mediator protein MDC1 is recruited to the DSB and binds γ-H2AX, where it promotes further ATM and MRN accumulation. As a consequence, γ-H2AX bidirectionally spreads out from the DSB (approximately 2 Mb), thus increasing the accumulation of repair factors. MDC1 also recruits RNF8/UBC13 ubiquitin ligase, which ubiquitinates H2A and H2AX, which, in turn, is recognized by RNF168-UBC13 H2AX-ubiquitin–ligase complex, resulting in the amplification of γ-H2AX polyubiquitination near the DSB. In parallel, γ-H2AX also permits TIP60 HAT recruitment at the break, followed by the acetylation of H2A and H4 histones, and destabilization of the nucleosomes. In addition, phosphorylation of H2AX could induce conformational changes in the nucleosome, resulting in the exposition of H4K20me and H3K79me, recognized by the checkpoint protein 53BP1.

How can this switch from prokaryotic DS break repair to eukaryotic DS break repair happen through a process of common descent without invoking simultaneous appearance of mechanisms to make it possible? It would be a statistical miracle.

Maybe you should study the biochemistry deeply before pretending to have it figured out. Studying in this context does not mean cutting and pasting written words and pretty cartoons.

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Maybe evolutionary biologists should, before claiming it evolved.

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Can you point to one claiming that this evolved with zero understanding of the biochemistry, Sal?

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They have, and it did. Willful ignorance by True Believers is not science’s problem.

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I wouldn’t say zero understanding, but rather inadequate understanding. I’d rather not mention names since he might be insulted, especially since I had more graduate biochem on chromatin than he did, and that’s not saying much.

You’re a legend in you own mind.

I don’t believe you. I’m talking about an understanding far deeper than any classroom variety. It’s not that hard.

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I guess they don’t teach about archaebacteria in the Gish School of Biological Sciences.

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It improves the average or mean reproductive success of the population when the least reproductively successful members of that population dies. That is not understood or purported to be an “improvement” for any individual in that population.

and selection often selects for damage, not for improvement as in numerous cases of reductive evolution

Selection is always for improvement in reproductive success. And in nothing else but that. What you consider “improvement” or “damage” is irrelevant. How does it affect reproductive success? That’s all that matters. Some times that is an increase in some measure of complexity, or number of molecular functions, other times it is not. And it is entirely possible that most molecular evolution is in that sense “degenerative”, where already existing functions are copied, become redundant, and eventually degrade. As a proportion of all molecular functions, it is entirely possible that most molecular changes are in that sense “losses” or “damage” of existing functions. But that isn’t actually a problem for any particular historical evolutionary trajectory, even those that imply the total number of molecular functions have increased, because it could have happened almost entirely by constructive neutral evolution in the manner I described.

Existing functions are multiplied (usually just by large duplications), are frequently entirely redundant even while strictly functional, and so eventually degrade again because they’re not maintained by purifying selection. And once in a rare while, a novel function emerges. The net amount of functional evolution is thus “degenerative” because those frequently copied but redundant functions are lost much more frequently than novel changes emerge, but the total complexity in terms of number of distinct molecular functions can still increase even under that kind of so-called degenerative evolution.

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That’s irrelevant since I never attended that school, and I was specifically describing a non-chromatin system in bacteria. One can state that some archaea have nucleosomes and chromatin-like architecture, but that doesn’t solve the problem of how DS break repair evolved in a chromatin system to begin with.

But, if you want to throw in archaea into the mix to explain chromatin and oddities like the helicases moving along the 3’-5’ polarity unlike bacteria, do you want to argue eukaryotes and archaea share a common ancestor that is separate form bacteria? Checkmate.

Is it an oddity or is it the norm for a protein that moves along a track to go in both directions?

Um, @stcordova, I was referring to your simplistic presentation of translation initiation. If you don’t know anything about the biochemistry involved (and you clearly don’t), the variability within and between the basic kingdoms (you are completely ignorant about this), the commonalities, and the deep evolutionary history that can be discerned from consideration of the structure of the ribosome (which comes from a rich and storied field you consider to be “bad science”), you are just making a fool of yourself here. Your Gish Gallop notwithstanding.

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Do you believe science has a reasonable model that explains this transition? Are you claiming there is no merit to Sals argument?

Sal’s “argument” is called the God of the Gaps fallacy and was rejected as worthless by science over 3 centuries ago Bill. You really need to come up to speed on this science stuff.

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The supposed transition is a figment of @stcordova’s imagination. The question I have is - is he deliberately misrepresenting things or is he just badly uninformed?

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Are you agreeing this is most likely a separate origin event?

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The transition from prokaryotes to eukaryotes?

No I am not.

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