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What Hacker News says
- I would encourage you to find a copy of (it's very expensive, but there are methods to acquire it, such as "libraries") Eugene Koonin's "The Logic of Chance", if this is a topic you're interested in. It basically goes through evolution from a molecular biology and information theory standpoint (and culminates in his own theory of "genesis").
- If anyone is interested in further reading on this topic, or on evolution/origin of life in general, I highly recommend "The Logic of Chance" by Eugene Koonin. The book pieces together the latest knowledge from all the major fields of biology (genetics/bioinformatics, structural/physics, etc), math, physics, and philosophy in a way I've never seen done before. It interrogates virtually every hypothesis of the origin of life, from all possible angles, starting mainly with what is evolution and what are the possible routes to where we are, as well as their probabilities, and critique of applying probability to these models.
I'm admittedly biased, because Koonin is a personal friend and occasional colleague of a member of my PhD committee, but what I've heard from everyone that I know who has interacted with him (unfortunately I've never had the opportunity, to my great dismay), is that he's completely unassuming and carries no ego at all. My experience reading "The Logic of Chance" has confirmed this. The book is accessible to anyone with an ability to read. It taught me more about how to think for myself and recognize bias than probably any other work I've read (perhaps excluding Taleb's "Incerto" series, which complement Koonin's work very nicely), and also taught me a lot about evolution. The book can be found on the usual websites that graduate students are apt to visit.
The RNA world hypothesis is almost single handedly responsible for my interest in virology.
- Look up the Logic of Chance by Eugene Koonin. Written by an actual evolution researcher of current times instead of legacy hacks like you-know-who.
This book is even better because it actually talks a lot of about horizontal gene transfer s role in prokaryotic evolution, and borgs might actually be something involved in a similar process. Kinda prescient if you ask me!
- I'm not an economist nor that interested in them, but I did read Nassim Taleb's books* and Kahneman stuck out as one of very few economists Taleb doesn't totally trash.
* I had read Eugene Koonin's "The Logic of Chance" and was then recommended Taleb's books for a more thorough perspective on probability, to apply to Koonin's work.
- I'm just doing a poor job of explaining what I'm trying to say , mainly because I was typing from my phone, and also because it's Friday evening after a long week and I've had a couple beers. And because a lot of this stuff is over my head.
Let me restate my issue with the OP in a clearer way and then I'll get into the rest of the nuance and detail.
OP said:
>there is evolutionary pressure [...] for coronaviruses to follow this path
I interpreted this line as reading: "coronaviruses will likely evolve furin sites because <some external force/evolution> is causing them to". The issue I take with it is that coronaviruses don't know what to evolve to, they simply evolve, and if it works, great. If not, they die. I'm not sure there's a cause beyond random/stochastic factors. Otherwise, it would be Lamarckian. If I were to reword it myself, I'd say "evolution of furin sites will be selected for". The reason I make this distinction is because elsewhere in the thread, I commented that a lab leak is a real hypothesis, and one of the counterarguments of that seems to be that because coronavirus could evolve a furin site without human intervention means that they did evolve a furin site without human intervention, and I dislike the narrative that it was an inevitability. (To make my position clear, I'd give a personal weighting of a natural evolution of Covid as about 85%, and a lab leak at about 14.9999999999%, and a malicious lab leak at about 0.000000000001%. Those numbers could be wildly off. I just get upset when people try to say a lab leak was definitely not possible).
>You understand the nuances better than most. I'm guessing you're self taught? I've never read the origin of species, but I feel like you might have!
I'd prefer to avoid a conversation based on credentials because of recent bad experiences there, but yes, I have read it. However, I was thinking about "The Logic of Chance" by Eugene Koonin, who is fairly well respected in the evolutionary biology field. Particularly, in "The Logic of Chance", he defines Lamarckian evolution as the following:
>Lamarckian inheritance refers to nonrandomly acquired phenotypic changes, particularly those that are directly affected by the use of organs and are accordingly assumed to be adaptive (beneficial for the organism). The controversial French naturalist Jean-Bapteste Lamarck believed that directed changes are inheritable and constitute the basis of evolution
He also goes on to say:
>Lamarck was the author of the first coherent theory of the evolution of life, which he presented in his Philosophie Zoologique; “inheritance of acquired (adaptive) characters” played a key role in this theory.
He makes a good, and much more nuanced argument than I'll attempt to explain here (see "The Logic of chance: The Nature and Origin of Biological Evolution, Chapter 9 for the full argument) that the inability of Lamarckian evolution only applies to the central dogma (DNA -> RNA -> Protein) because the central dogma has no reverse mechanism (no way to transfer information from protein back to DNA). However, this scenario falls apart with the advent of things like proteins that can insert novel DNA into a genome, or reverse-transcriptases.
Specifically regarding CRISPR/Cas, Koonin has this to say: >The mechanism of heredity and genome evolution embodied in the CRISPR-Cas system seems to be bona fide Lamarckian (see Figure 9-2):
>• An environmental cue (a selfish genetic element, such as a virus) is employed to directly modify the genome.
>• The resulting modification (unique, element-specific spacer) directly affects the same cue that caused the modification.
>• The modification is clearly adaptive and is inherited by the progeny of the cell that encountered the selfish element.
He goes on to address your points about losing with disuse, as well:
>The CRISPR-mediated heredity appears to be short-lived: Even closely related bacterial and archaeal genomes do not carry the same inserts. The implication is that, as soon as a bacterium or archaeon ceases to encounter a particular agent (virus), the cognate spacer rapidly deteriorates.
While "Logic of Chance" was written in 2013, if I remember correctly, which was the nascent stages of CRISPR/Cas understanding, my personal experience in biology has proven that to be quite true. We know now that CRISPR spacers are inserted into the beginning of the spacer locus, directly adjacent the leader which is where spacer transcription is initiated, and this apparently serves an evolutionary function of ensuring that the transcription guarantees more transcripts of the most recently encountered viruses.
That said, there are some serious flaws in his thinking. See this rebuttal:
https://link.springer.com/article/10.1007/s10539-018-9662-y
As always, in large part, the phenomena is undisputed, and the fact that it breaks the central dogma is...mostly...undisputed, but the actual definition of the term "Lamarckian" is in hot dispute.
(See also Koonin's response to that rebuttal here: https://link.springer.com/article/10.1007/s10539-018-9666-7)
I appreciate the thoughtful discussion.
- Your numbers appear to be off.
There are about 25k unique protein coding genes in the human genome, not 500k.
Additionally, there appears to be a size limit to proteins. The largest human protein, titin, is about 40k amino acids. No larger protein has ever been discovered.
Obviously 20^40000 is an incomprehensible coding space, but we can with a few broad strokes narrow that number down immensely.
For starters, Eugene Koonin argues in The Logic of Chance, and elsewhere, that the evolution of proteins is limited by the amount of stable folds available in cell-like aqueous conditions. It's an impossible number to quantify but we do know that even most cellular proteins will naturally misfold coming off the ribosome unless aided by chaperones, so we can assume that coding space is drastically decreased.
Furthermore, because of inertia, there are many combinations evolution simply will not sample. Most genes evolve by genome duplication events. The conclusion of the process is that youre never going to get too far away from what you stated with, and indeed we see this is the case with there only being a handful of true, conserved orthogonal genes (these number in the hundreds).
Obviously, n = 1, but I guess the point I'm trying to make is that once you have stable structure/function chemistry, there's probably many many routes to "humans" or something else able to be self aware. We just see one of them because of we were guided here by earth chemistry and inertia.
What is far more confusing is how the ribosome evolved in the first place, because that's the true de novo lynchpin of cellular life.
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