Re: Life: Turn it upside down!

On 10/04/2024 07:58, Arkalen wrote:

On 09/04/2024 23:41, Ernest Major wrote:

On 09/04/2024 19:17, Arkalen wrote:

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Sorry, I thought you'd excluded viruses with the "step down from there" bit. The gulf is still huge between viruses and cellular life but I guess it's true the gulf between cellular life and nonlife is smaller if you include them. The issue in terms of abiogenesis is that it's unclear whether they're true intermediates or if they arose after or parallel to cellular life.

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It's conceivable that all three models for the origins of viruses (relicts of pre-cellular life, highly reduced descendants of parasitic cells, rogue genes) are true, for different groups of viruses.
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Mimivirus has a bigger genome and more genes than some cellular organisms, including some genes involved in metabolism and in protein synthesis. This, and nucleocytoplasmic large DNA viruses in general, seem to go some of the way in filling the gap between viruses in general and cellular organisms.
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 I agree with all of that. Just to clarify: when I talk about the huge gulf in complexity between viruses and cellular life I'm not talking about genome size, I'm talking very specifically about everything cellular life is that viruses aren't, with cellular structure & components, metabolism, translation mechanisms, all the resulting behavior... I don't think even mimivirus begins to compete in that field but I'm happy to learn more.
 

I don't know what mimivirus does with all its genome. The following may give an idea of how much is actually known. (It's more than I expected.)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9133948/
Autotrophs have "complete" metabolisms. Heterotrophs need not. For example, human lack the ability to synthesis essential amino acids and various essential metabolic cofactors (aka vitamins). Parasites, especially intracellular parasites (including parasitic plants, which invade their hosts at the intracellular level) lack even more of the metabolism, scavenging chemicals from their hosts. With 1,000 or so genes, mimivirus also has a truncated metabolism (I don't know how it compares to say Wolbachia, but with comparable numbers of genes a comparison seems an obvious thing to investigate.) A difference between mimiviruses and intracellular parasites is that the latter have their own cytoplasm, while the former utilises the host cytoplasm as a substrate for its metabolism. That's still a big difference - but is it the only difference in kind between mimiviruses and the simplest intracellular parasitic organisms? (According to the above paper mimivirus has an immune system, which is something one could imagine a cellular organism lacking.)
One can imagine an intermediate condition - where the parasite has its own cytoplasm, but also exports enzymes into the host cytoplasm to extend its metabolism into the host cytoplasm. (At a grosser scale venoms are somewhat analogous, but being associated with predation rather than parasitism are purely destructive. However fungal parasites modify the behaviour of their hosts may be getting closer to this intermediate, though I suspect this also is more interference with the host metabolism rather than parasitising it.)
A contrary hypothesis is that large parts of the mimivirus genome are junk DNA - remnants not yet eliminated of a ancestral cellular state, or alternatively host genes accidentally incorporated in the mimivirus genome, the retention of which is permitted by the large size of the mimivirus capsid. I would expect that mimiviruses, like bacteria, would be under effective selection for the removal of superfluous DNA, but one could postulate a structural role - the excess DNA serving as packing to maintain the integrity of the capsid. There is a wide variety of genome sizes among mimivirus and its relatives, which would seem to allow this hypothesis to be tested by looking for a correlation between capsid volume and genome size.
--
alias Ernest Major