possible roots of procaryote-eucaryote relations, bearing on immunity

[Guest guest]

In some mammal cell types, mitochondrial membrane damage, releasing

various factors, is an essential part of the cell suicide cascade.

This step may not be essential to suicide in other cell types, but

may happen anyway. During apoptotic signaling, various cytoplasmic

proteins from the mammal genome act to damage or protect

mitochondrial membranes. Key membrane-damaging pro-apoptotic

proteins are very potently degraded by Chlamydia trachomatis to

protect human endothelial cells from artificially-induced apoptosis

in vitro (Zhong G 2005). Which may be crucial to persistance of

chlamydia, and conceivably other intracellular pests, in vivo.

Genes for these proteins may have been captured by eucaryotes from

the proto-mitochondria themselves. Phylogenetic evidence for this is

presented in this article. A possible history of the interaction is

proposed in the epilogue, copied below:

http://www.nature.com/cgi-taf/DynaPage.taf?file=/cdd/journal/v9/n4/full/4400991a\

..html

" After submission of the manuscript of this study, it came to our

attention that mitochondrial endosymbiosis and the origin of

eukaryotic PCD [programmed cell death] could be linked in a

straightforward hypothesis. The early alpha-proteobacterial

endosymbionts might have been using secreted and membrane proteases,

such as metacaspases, paracaspases and HtrA-like proteases, to kill

their host cells once those became unhospitable environments, e.g.

because of scarcity of nutrients. Such a mechanism could enable the

endosymbionts to efficiently use the corpse of the assassinated host

and move to another host. During subsequent evolution, this weapon

of aggression might have been appropriated by the host and made into

a means of programmed suicide, with the subsequent addition of

regulatory components. In general terms, this idea has been proposed

by Frade and idis (Frade JM, idis TM (1997) Origin of

eukaryotic programmed cell death: a consequence of aerobic

metabolism? Bioessays 19: 827-832). "

Consider that we are talking about unicellular proto-eucaryote hosts

here, so killing the host cell will not expose parasites to immune

system componants - only to the open environment they came from. The

life processes of the host can benefit parasites, but at a certain

point this might be outweighed by the strain on the parasites from

defensive host chemistry changes and the potential benefit to the

parasites of dispersing into new hosts. At that point they secrete

factors that kill the host.

The genetics of this machinery is eventually captured by

proto-eucaryotes - perhaps because kin selection stably favors their

rapid apoptosis upon infection, as proffered here:

http://www.nature.com/cgi-taf/DynaPage.taf?file=/cdd/journal/v9/n4/full/4400986a\

..html

What a brilliant move by proto-eucaryotes - by " stealing " the

capability for apoptosis their immunity is vastly improved (not the

immunity of individual cells of course, but that of clones, or sets

of related clones, existing in proximity). As a small bonus

apoptosis even allows them to develop successful multicellularity.

But the procaryotes strike back, possibly perpetuating infection

largely by means of secreted factors that interfere with apoptosis.

And then what?

Interestingly, some procaryotes are parasitised by fellow

procaryotes such as Bdellovibrio. The immense majority of

procaryotes are undescribed so there might be alot more. I wonder if

any procaryote hosts have developed cell suicide, unbeknownst as yet

to science.

[Guest guest]

you're having a good time eric . you're keeping your mind awake and

alive.

an interesting fact about epidemics is the virulence of an infection

decreases over time, host and pathogen adapt to each other. why is

that. maybe to some extent in the beginning you just kill off the

weaker ones (genetically). but also the more successful pathogen is

one that can live with its host and be transmitted. so maybe there is

selective pressure on the pathogen that way.

i don't know what that means for lyme because tbd are bioweaponized (i

believe) but i guess eventually, it would mean they became less

virulent.