AI Article Synopsis
- Vibrio cholerae, which causes cholera, has a curved rod shape that aids its infectivity and movement in dense environments.
- The small RNA VadR regulates the gene crvA responsible for this curvature; mutations to vadR lead to increased cell curvature, while overexpression reduces it.
- VadR is activated by the VxrAB system and is crucial for maintaining cell shape, antibiotic resistance, and inhibiting biofilm formation in V. cholerae.
Article Abstract
Vibrio cholerae, the cause of cholera disease, exhibits a characteristic curved rod morphology, which promotes infectivity and motility in dense hydrogels. Periplasmic protein CrvA determines cell curvature in V. cholerae, yet the regulatory factors controlling CrvA are unknown. Here, we discover the VadR small RNA (sRNA) as a post-transcriptional inhibitor of the crvA mRNA. Mutation of vadR increases cell curvature, whereas overexpression has the inverse effect. We show that vadR transcription is activated by the VxrAB two-component system and triggered by cell-wall-targeting antibiotics. V. cholerae cells failing to repress crvA by VadR display decreased survival upon challenge with penicillin G indicating that cell shape maintenance by the sRNA is critical for antibiotic resistance. VadR also blocks the expression of various key biofilm genes and thereby inhibits biofilm formation in V. cholerae. Thus, VadR is an important regulator for synchronizing peptidoglycan integrity, cell shape, and biofilm formation in V. cholerae.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695739 | PMC |
| http://dx.doi.org/10.1038/s41467-020-19890-8 | DOI Listing |
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