Pseudomonas aeruginosa cleaves the decoding center of Caenorhabditis elegans ribosomes
dc.contributor.author | Vasquez-Rifo, Alejandro | |
dc.contributor.author | Ricci, Emiliano P. | |
dc.contributor.author | Ambros, Victor R. | |
dc.date | 2022-08-11T08:09:57.000 | |
dc.date.accessioned | 2022-08-23T16:50:25Z | |
dc.date.available | 2022-08-23T16:50:25Z | |
dc.date.issued | 2020-12-01 | |
dc.date.submitted | 2020-12-30 | |
dc.identifier.citation | <p>Vasquez-Rifo A, Ricci EP, Ambros V. Pseudomonas aeruginosa cleaves the decoding center of Caenorhabditis elegans ribosomes. PLoS Biol. 2020 Dec 1;18(12):e3000969. doi: 10.1371/journal.pbio.3000969. PMID: 33259473; PMCID: PMC7707567. <a href="https://doi.org/10.1371/journal.pbio.3000969" target="_blank" title="article on publisher's site">View article on publisher's site</a></p> | |
dc.identifier.issn | 1545-7885 | |
dc.identifier.doi | 10.1371/journal.pbio.3000969 | |
dc.identifier.pmid | 33259473 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/41655 | |
dc.description.abstract | Pathogens such as Pseudomonas aeruginosa advantageously modify animal host physiology, for example, by inhibiting host protein synthesis. Translational inhibition of insects and mammalian hosts by P. aeruginosa utilizes the well-known exotoxin A effector. However, for the infection of Caenorhabditis elegans by P. aeruginosa, the precise pathways and mechanism(s) of translational inhibition are not well understood. We found that upon exposure to P. aeruginosa PA14, C. elegans undergoes a rapid loss of intact ribosomes accompanied by the accumulation of ribosomes cleaved at helix 69 (H69) of the 26S ribosomal RNA (rRNA), a key part of ribosome decoding center. H69 cleavage is elicited by certain virulent P. aeruginosa isolates in a quorum sensing (QS)-dependent manner and independently of exotoxin A-mediated translational repression. H69 cleavage is antagonized by the 3 major host defense pathways defined by the pmk-1, fshr-1, and zip-2 genes. The level of H69 cleavage increases with the bacterial exposure time, and it is predominantly localized in the worm's intestinal tissue. Genetic and genomic analysis suggests that H69 cleavage leads to the activation of the worm's zip-2-mediated defense response pathway, consistent with translational inhibition. Taken together, our observations suggest that P. aeruginosa deploys a virulence mechanism to induce ribosome degradation and H69 cleavage of host ribosomes. In this manner, P. aeruginosa would impair host translation and block antibacterial responses. | |
dc.language.iso | en_US | |
dc.publisher | Public Library of Science | |
dc.relation | <p><a href="https://pubmed.ncbi.nlm.nih.gov/33259473/" target="_blank" title="view article in PubMed">View article in PubMed</a></p> | |
dc.rights | Copyright: © 2020 Vasquez-Rifo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.subject | Pseudomonas aeruginosa | |
dc.subject | Ribosomal RNA | |
dc.subject | Caenorhabditis elegans | |
dc.subject | Ribosomes | |
dc.subject | Virulence factors | |
dc.subject | Biochemistry, Biophysics, and Structural Biology | |
dc.subject | Biology | |
dc.subject | Developmental Biology | |
dc.subject | Pathogenic Microbiology | |
dc.title | Pseudomonas aeruginosa cleaves the decoding center of Caenorhabditis elegans ribosomes | |
dc.type | Journal Article | |
dc.source.journaltitle | PLoS biology | |
dc.source.volume | 18 | |
dc.source.issue | 12 | |
dc.identifier.legacyfulltext | https://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=5476&context=oapubs&unstamped=1 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/oapubs/4446 | |
dc.identifier.contextkey | 20879127 | |
refterms.dateFOA | 2022-08-23T16:50:25Z | |
html.description.abstract | <p>Pathogens such as Pseudomonas aeruginosa advantageously modify animal host physiology, for example, by inhibiting host protein synthesis. Translational inhibition of insects and mammalian hosts by P. aeruginosa utilizes the well-known exotoxin A effector. However, for the infection of Caenorhabditis elegans by P. aeruginosa, the precise pathways and mechanism(s) of translational inhibition are not well understood. We found that upon exposure to P. aeruginosa PA14, C. elegans undergoes a rapid loss of intact ribosomes accompanied by the accumulation of ribosomes cleaved at helix 69 (H69) of the 26S ribosomal RNA (rRNA), a key part of ribosome decoding center. H69 cleavage is elicited by certain virulent P. aeruginosa isolates in a quorum sensing (QS)-dependent manner and independently of exotoxin A-mediated translational repression. H69 cleavage is antagonized by the 3 major host defense pathways defined by the pmk-1, fshr-1, and zip-2 genes. The level of H69 cleavage increases with the bacterial exposure time, and it is predominantly localized in the worm's intestinal tissue. Genetic and genomic analysis suggests that H69 cleavage leads to the activation of the worm's zip-2-mediated defense response pathway, consistent with translational inhibition. Taken together, our observations suggest that P. aeruginosa deploys a virulence mechanism to induce ribosome degradation and H69 cleavage of host ribosomes. In this manner, P. aeruginosa would impair host translation and block antibacterial responses.</p> | |
dc.identifier.submissionpath | oapubs/4446 | |
dc.contributor.department | Program in Molecular Medicine | |
dc.source.pages | e3000969 |