Vibrio cholerae O1 biovar El Tor str. N16961
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA295519 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
Project description:Replication control in Vibrio cholerae
| PRJNA311520 | ENA
Project description:Vibrio cholerae N16961 overexpression of CpxR
| PRJNA234543 | ENA
Project description:Mutation-accumulation Lines of Vibrio cholerae N16961
| PRJNA383052 | ENA
Project description:Vibrio cholerae Transcriptome/SOS induction differential transcription screen
| PRJNA429784 | ENA
Project description:Effect of cFP on gene expression in Vibiro cholerae
| PRJNA167506 | ENA
Project description:Vibrio cholerae O1 biovar El Tor str. N16961 Transcriptome or Gene expression
| PRJNA295073 | ENA
Project description:MerR and ChrR mediate blue light induced photo-oxidative stress response at the transcriptional level in Vibrio cholerae
| PRJNA317358 | ENA
Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxR’s genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. cholerae’s major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites.
2016-03-23 | GSE72473 | GEO
Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxR’s genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. cholerae’s major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites.
2016-03-23 | GSE72472 | GEO