Greetings fellow eukaryotes,
I really enjoyed your recent coverage of the paper on bacterial cell wall shedding from Ariane Briegel and Dennis Claessen last week. I am currently working on a project involving bacillus phage phi29 in Ethan Garner’s lab at Harvard, so I have been thinking about this paper constantly since it came out.
There is something you missed though: at almost the same time that paper was published, Martin Loessner’s group posted a preprint entitled Gram-positive bacteria evade phage predation through endolysin-mediated L-form conversion. In addition to confirming the existence of the effect by observing it in two other species, Listeria monocytogenes and Enterococcus faecalis, they specifically address the question of whether this would happen in natural environments. Enterococcus is a cause of urinary tract infections, and it turns out urine is osmoprotective- they show directly that cell wall loss can happen in human urine! Very cool, though disappointing for the prospects of using phage therapy on that particular bug.
There is also an interesting disagreement about phage lysins. As you mentioned, the Briegel/Claessen paper claimed that lysins do not drive cell wall loss because they could not observe it when adding filtered lysate directly to cells. The Loessner paper, on the other hand, manufactured highly purified lysins and was able to demonstrate that they could induce cell wall loss. It is unclear to me which is more relevant! At first, the lysate sounds like a much more natural test of physiological conditions. However, in a natural phage infection on a solid surface, the local concentration of lysins diffusing to the neighbor of a phage-infected cell is presumably much higher than the concentration of lysins well-mixed in liquid culture.
Finally- in your discussion, you attribute the cell wall loss to selection. But under the osmoprotective conditions, the cell wall loss is rapid, happens in most cells, and is reversible, none of which is what you would expect from phage resistance by selection (like, say, having a mutation in the receptor the phage binds to). In fig 1a of Loessner for instance, they point out individual cells making the transition. Something else is going on here, whether it’s just the action of the lysins or a more sophisticated response driven by the bacteria themselves.