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Vibrio cholerae O1 biovar El Tor str. N16961

ABSTRACT: Replication control in Vibrio cholerae

PROVIDER: PRJNA311520 | ENA |

REPOSITORIES: ENA

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Comparative whole cell proteomics data of Vibrio cholerae O1 biovar El Tor str. N16961 versus full length cgtA knockdown and CgtA(∆CTD) during nutrient limiting condition

Project description:Adapting to nutritional downshifts is crucial for the survival of Vibrio cholerae. CgtA, a 50S ribosome-associated essential GTPase, is a bonafide stringent response protein. CgtA, in association with SpoT, modulates the intracellular (p)ppGpp alarmone levels in a nutrient-rich environment. We studied the influence of CgtA during the growth of V. cholerae in a minimal medium in contrast to its pre-defined role in a nutrient-rich medium. Here, we show the pleiotropic effects of CgtA on growth, viability, motility, morphology, and persister phenotype of a V. cholerae strain where the full-length wildtype (Wt) cgtA was deleted. An in-frame deletion of the 52 amino acids long unstructured C-terminal domain of the CgtA GTPase defined its in vivo functionality. Proteomic analyses revealed that loss of CgtA significantly altered 311 proteins involved in diverse cellular processes. However, the CgtA C-terminus deleted strain altered 240 proteins with a major overlap with the full-length cgtA deleted condition. A sustained mRNA expression pattern of CgtA is observed in a minimal medium. Whereas, in nutrient-rich LB medium, intermittent expression of cgtA is observed with the highest expression during the late-logarithmic to early-stationary phase. We propose that minimal media-associated nutrient stress coupled to cgtA depletion aggravates the intracellular stress in V. cholerae, leading to abnormal protein synthesis, altered DNA replication, and transcriptional machinery, negatively affecting cellular energy metabolism and many vital processes. This study suggests that the nutrient-media-dependent controlled expression of CgtA is a mechanism by which V. cholerae can remodel its transcriptome and proteome. Our study reveals an alternative facet of the survival of V. cholerae during nutritional downshift and the consequences concomitantly with cgtA knockdown as evident from the complex altered regulatory network.

2023-03-03 | PXD034015 | Pride

Vibrio cholerae O1 biovar El Tor str. N16961

Project description:Vibrio cholerae N16961 overexpression of CpxR

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Vibrio cholerae strain:O1 biovar El Tor N16961

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Analysis of ToxT regulon in Vibrio cholerae El Tor

Project description:Using a combination of ChIP-seq and RNA-seq we show that ToxT regulates expression of the small RNA TarB. TarB modulates the expression level of the transcriptioanl repressor VC0177. VC0177 controls expression of several genes including VC0179. The function of the Vibrio 7th pandemic island-1 (VSP-1) in cholera pathogenesis has remained obscure. Utilizing ChIP-seq and RNA-seq to map the regulon of the master virulence regulator ToxT, we identify a TCP island encoded small RNA that reduces the expression of a previously unrecognized VSP-1 encoded transcription factor termed VspR. VspR modulates the expression of several VSP-1 genes including one that encodes a novel class of di-nucleotide cyclase (DncV), which preferentially synthesizes a previously undescribed hybrid cyclic AMP-GMP molecule. We show that DncV is required for efficient intestinal colonization and down-regulates V. cholerae chemotaxis, a phenotype previously associated with hyperinfectivity. This pathway couples the actions of previously disparate genomic islands, defines VSP-1 as a pathogenicity island in V. cholerae and implicates its occurrence in 7th pandemic strains as a benefit for host adaptation through the production of a regulatory cyclic di-nucleotide.

2012-04-13 | E-GEOD-36373 | biostudies-arrayexpress

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