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Pseudomonas aeruginosa cleaves the decoding center of Caenorhabditis elegans ribosomes.

Alejandro Vasquez-Rifo, Emiliano P Ricci, and Victor Ambros (2020)

PLoS Biol, 18(12):e3000969.

Pathogens such as Pseudomonas aeruginosa advantageously modify animal hostphysiology, for example, by inhibiting host protein synthesis. Translationalinhibition of insects and mammalian hosts by P. aeruginosa utilizes the well-knownexotoxin A effector. However, for the infection of Caenorhabditis elegans by P.aeruginosa, the precise pathways and mechanism(s) of translational inhibition arenot well understood. We found that upon exposure to P. aeruginosa PA14, C. elegansundergoes a rapid loss of intact ribosomes accompanied by the accumulation ofribosomes cleaved at helix 69 (H69) of the 26S ribosomal RNA (rRNA), a key part ofribosome decoding center. H69 cleavage is elicited by certain virulent P. aeruginosaisolates in a quorum sensing (QS)-dependent manner and independently of exotoxinA-mediated translational repression. H69 cleavage is antagonized by the 3 major hostdefense pathways defined by the pmk-1, fshr-1, and zip-2 genes. The level of H69cleavage increases with the bacterial exposure time, and it is predominantlylocalized in the worm's intestinal tissue. Genetic and genomic analysis suggeststhat H69 cleavage leads to the activation of the worm's zip-2-mediated defenseresponse pathway, consistent with translational inhibition. Taken together, ourobservations suggest that P. aeruginosa deploys a virulence mechanism to induceribosome degradation and H69 cleavage of host ribosomes. In this manner, P.aeruginosa would impair host translation and block antibacterial responses.

 
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