Talmudic Question #41

Bacteria are prey to bacteriophages, other bacteria, protists, and fungi. Can you think of a mechanism that all these predators may have in common?

Bacteria are prey to bacteriophages, other bacteria, protists, and fungi. Can you think of a mechanism that all these predators may have in common?
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CONTACT!
In order to eat one has to touch! There has to be surface to surface contact in order to engulf! Thus, we could generalize and say that all predators have to contact their prey! This is one of the key common mechanisms. The claw and teeth of the lion has to contact the antelope, just like lambda to bacterial OMP's, fungal hyphae to cell surface receptors, ad infinitum...
However, on might envision death without direct engagement – such as by long distance toxins – and then absorbance of the nutrients released. This latter matter has two philosophical problems in regard to the Talmudic question asked. First, long distance killing by toxins does not necessarily mean absorption of nutrient. Thus its a "predator in trans". Secondly, even a toxin has to make contact eventually, thus not eliminating the common mechanism of contact – in its most orthodox understanding.
The predator sends a message, "are you friend or foe?" If foe, the predator recognizes foe via peptide/polysaccharide, and attacks. This is what phage and other predators have in common. See papers by Bettelheim who explains friend/foe recognition.
Colony incompatibility studies of enterotoxigenic Escherichia coli O126 isolated during one outbreak.
Bettelheim KA.
J Clin Microbiol. 1984 Mar;19(3):408–11.
Colony incompatibility in bacteria.
Bettelheim KA, Carlile MJ.
Nature. 1976 Dec 23–30;264(5588):757–8. No abstract available.
See also Prophage contribution to bacterial population
dynamics.
Bossi, et al.
J. Bacteriology 2003 185: 6461–71.
The real issue, over and over, is self versus nonself. Look at the issue of "cheaters" in Greg Velicer's work with myxobacters.
Travisano, M. and G.J. Velicer (2004). "Strategies of microbial cheater control." Trends Microbiol. 12: 72 — 78.
"Cheating" applies to all kind of microbe-microbe interactions, after all.
I haven't actually sat down and done the experiment, but does a given strain of Bdellovibrio "prefer" other bacteria to its sibs? Interesting question, but it remains important to keep in mind that what we "set up" in the laboratory does not reflect the natural situation very closely. It reminds me very much of my old system of Sinorhizobium meliloti and alfalfa—mutant bacteria added to bare roots on agar, and drawing conclusions about nodulation effects. The lab found out a great deal, but the interplay of the diverse rhizosphere microbiota is a tough nut to crack. Hence my thinking about "cheaters."
The "dead hand" of Darwin is ever with us. And to borrow from J.B.S. Haldane, I don't believe that the microbial world is merely stranger than we imagine. It is stranger than we can imagine.
I particularly appreciate seeing references here to "old" papers that genome-philes may have missed. The most important instrument in a laboratory is not a fancy qPCR thermocycler, but eyes and brain. This paper reminds me of that principle:
Shuman, H.A. (2003). "Just toothpicks and logic: how some labs succeed at solving complex problems." J. Bacteriol. 185: 387 — 390 (with three cheers for Jon Beckwith, who, like Elio and several other posters here, has forgotten more than I will ever know about microbial genetics).
Oh...and happy Thanksgiving to all microphiles, near and far.
Elio, I am vacationing with my family in Long Beach, Washington, and thought of you when I saw not one but two "mushroom hunting" guides in the gift shop of our hotel. Well, I am actually grading papers, but you know what I mean.