Similar Datasets
Project description:Caulobacter species are dimorphic Gram-negative bacteria that inhabit diverse terrestrial and aquatic ecosystems. A suite of molecular sensory systems enables these microbes to control growth, development, and reproduction in response to levels of essential elements, including carbon, nitrogen, and phosphorus. Although the enhancer binding protein NtrC and its cognate sensor histidine kinase NtrB are well-established regulators of bacterial nitrogen assimilation, their precise functions in Caulobacter metabolism and cell development remained largely undefined. Deletion of C. crescentus ntrC slowed cell growth in complex medium, while ntrB and ntrC were essential for growth when ammonium was the sole nitrogen source due to their requirement for glutamine synthase (glnA) expression. Random transposition of a conserved IS3-family mobile genetic element frequently rescued the growth defect of ntrC mutant strains by restoring glnBA transcription, revealing a possible role for IS3 transposition in shaping the evolution of Caulobacter populations during nitrogen limitation. We further defined the NtrC regulon through transcriptomic and ChIP-seq analyses, which demonstrated the role of NtrC as both a transcriptional activator and repressor. The chromosome of C. crescentus harbors dozens of direct binding sites for NtrC, with a significant proportion located near genes involved in polysaccharide biosynthesis. Numerous NtrC binding sites align with those of GapR, an essential protein involved in chromosome organization, and MucR1, a cell cycle regulator. This observation suggests that NtrC participates in the regulation of cell cycle and cell development. Indeed, loss of NtrC function led to elongated polar stalks and elevated synthesis of cell envelope polysaccharides. These developmental defects were restored by supplementing media with glutamine or by ectopic expression of the glnBA operon. This study establishes a regulatory connection between NtrC, nitrogen metabolism, polar morphogenesis, and envelope polysaccharide synthesis in Caulobacter.
2023-06-07 | GSE234096 | GEO
Project description:Caulobacter species are dimorphic Gram-negative bacteria that inhabit diverse terrestrial and aquatic ecosystems. A suite of molecular sensory systems enables these microbes to control growth, development, and reproduction in response to levels of essential elements, including carbon, nitrogen, and phosphorus. Although the enhancer binding protein NtrC and its cognate sensor histidine kinase NtrB are well-established regulators of bacterial nitrogen assimilation, their precise functions in Caulobacter metabolism and cell development remained largely undefined. Deletion of C. crescentus ntrC slowed cell growth in complex medium, while ntrB and ntrC were essential for growth when ammonium was the sole nitrogen source due to their requirement for glutamine synthase (glnA) expression. Random transposition of a conserved IS3-family mobile genetic element frequently rescued the growth defect of ntrC mutant strains by restoring glnBA transcription, revealing a possible role for IS3 transposition in shaping the evolution of Caulobacter populations during nitrogen limitation. We further defined the NtrC regulon through transcriptomic and ChIP-seq analyses, which demonstrated the role of NtrC as both a transcriptional activator and repressor. The chromosome of C. crescentus harbors dozens of direct binding sites for NtrC, with a significant proportion located near genes involved in polysaccharide biosynthesis. Numerous NtrC binding sites align with those of GapR, an essential protein involved in chromosome organization, and MucR1, a cell cycle regulator. This observation suggests that NtrC participates in the regulation of cell cycle and cell development. Indeed, loss of NtrC function led to elongated polar stalks and elevated synthesis of cell envelope polysaccharides. These developmental defects were restored by supplementing media with glutamine or by ectopic expression of the glnBA operon. This study establishes a regulatory connection between NtrC, nitrogen metabolism, polar morphogenesis, and envelope polysaccharide synthesis in Caulobacter.
2023-06-07 | GSE234095 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2016-12-21 | GSE87173 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-04-11 | GSE200466 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2015-06-13 | E-GEOD-69848 | biostudies-arrayexpress
Project description:A conserved set of regulators control the general stress response in Caulobacter crescentus, including ?(T), its anti-? factor NepR, the anti-anti-? factor PhyR, and the transmembrane sensor kinase PhyK. We report that the soluble histidine kinase LovK and the single-domain response regulator LovR also function within the C. crescentus general stress pathway. Our genetic data support a model in which LovK-LovR functions upstream of ?(T) by controlling the phosphorylation state and thus anti-anti-? activity of PhyR. Transcription of lovK and lovR is independently activated by stress through a mechanism that requires sigT and phyR. Conversely, lovK and lovR function together to repress transcription of the general stress regulon. Concordant with a functional role of the LovK-LovR two-component system as a negative regulator of the general stress pathway, lovK-lovR-null mutants exhibit increased cell survival after osmotic stress, while coordinate overexpression of lovK and lovR attenuates cell survival relative to that of the wild type. Notably, lovK can complement the transcriptional and cell survival defects of a phyK-null mutant when lovR is deleted. Moreover, in this same genetic background, ?(T)-dependent transcription is activated in response to osmotic stress. This result suggests that flavin-binding LOV (light, oxygen, or voltage) histidine kinases are competent to perceive cytoplasmic signals in addition to the environmental signal blue light. We conclude that the PhyK-PhyR and LovK-LovR two-component signaling systems coordinately regulate stress physiology in C. crescentus.
| S-EPMC3370868 | biostudies-literature
Project description:Despite the well-known toxicity of uranium (U) to bacteria, little is known about how cells sense and respond to U. The recent finding of a U-specific stress response in Caulobacter crescentus has provided a foundation for studying the mechanisms of U- perception in bacteria. To gain insight into this process, we used a forward genetic screen to identify the regulatory components governing expression of the urcA promoter (PurcA) that is strongly induced by U. This approach unearthed a previously uncharacterized two-component system, UzcRS, which is responsible for U-dependent activation of PurcA. UzcRS is also highly responsive to zinc and copper, revealing a broader specificity than previously thought. Using ChIP-seq, we found that UzcR binds extensively throughout the genome in a metal-dependent manner and recognizes a non-canonical DNA binding site. Coupling the genome-wide occupancy data with RNA-seq analysis revealed that UzcR is a global regulator of transcription, predominately activating genes encoding proteins that are localized to the cell envelope; these include metallopeptidases, multidrug resistant efflux (MDR) pumps, TonB-dependent receptors and many proteins of unknown function. Collectively, our data suggest that UzcRS couples detection of U, Zn and Cu with a novel extracytoplasmic stress response.
2016-12-21 | GSE87172 | GEO
Project description:Despite the well-known toxicity of uranium (U) to bacteria, little is known about how cells sense and respond to U. The recent finding of a U-specific stress response in Caulobacter crescentus has provided a foundation for studying the mechanisms of U- perception in bacteria. To gain insight into this process, we used a forward genetic screen to identify the regulatory components governing expression of the urcA promoter (PurcA) that is strongly induced by U. This approach unearthed a previously uncharacterized two-component system, UzcRS, which is responsible for U-dependent activation of PurcA. UzcRS is also highly responsive to zinc and copper, revealing a broader specificity than previously thought. Using ChIP-seq, we found that UzcR binds extensively throughout the genome in a metal-dependent manner and recognizes a non-canonical DNA binding site. Coupling the genome-wide occupancy data with RNA-seq analysis revealed that UzcR is a global regulator of transcription, predominately activating genes encoding proteins that are localized to the cell envelope; these include metallopeptidases, multidrug resistant efflux (MDR) pumps, TonB-dependent receptors and many proteins of unknown function. Collectively, our data suggest that UzcRS couples detection of U, Zn and Cu with a novel extracytoplasmic stress response.
2016-12-21 | GSE87171 | GEO
Project description:This experiment is testing the effects of coordinate overexpression of the lovK-lovR two-component system on gene expression in Caulobacter crescentus relative to an empty vector control strain.
2012-06-01 | GSE21204 | GEO
Project description:Two-component systems (TCS) are often used by bacteria to rapidly assess and respond to environmental changes. ChvG/ChvI (ChvGI) is a TCS conserved in γ-proteobacteria and is known for regulating expression of genes related to exopolysaccharide production, virulence and growth. The sensor kinase ChvG autophosphorylates upon yet unknown signals and phosphorylates the response regulator ChvI to activate transcription. Recent studies in Caulobacter crescentus showed that chv mutants are sensitive to vancomycin treatment and fail to grow in synthetic minimal media. In this work, we identified the osmotic imbalance as the main cause of growth impairment in synthetic minimal media. We also determined the ChvI regulon and confirmed that ChvI regulates cell envelope architecture at different levels by controlling outer membrane, peptidoglycan assembly/recycling and inner membrane proteins. Furthermore, we identified genes with osmoregulatory properties and confirmed that osmotic upshift is a signal triggering ChvG-dependent phosphorylation of ChvI. In addition, we challenged chv mutants with other cell envelope related stress and found that targeting with antibiotics the transpeptidation of peptidoglycan during cell elongation impairs growth of the mutant. Moreover, these antibiotics activate expression of the chvIG-hprK operon in ChvI-dependent and independent ways. ChvI phosphorylation is also shown to be activated upon antibiotic treatment with vancomycin. Finally, we observed that the sensor kinase ChvG fused to a fluorescent protein relocates from a patchy-spotty distribution to distinctive foci after transition from complex to synthetic minimal media. Interestingly, this pattern of (re)location has been described for proteins involved in cell growth control and peptidoglycan synthesis upon osmotic shock. Overall, our data support that the ChvGI TCS is mainly used to monitor and respond to osmotic imbalances and damages in the peptidoglycan layer.
2022-04-11 | GSE200465 | GEO