Elucidating transcriptional regulation of nitrogen metabolism with systems approaches [ChIP-Seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Escherichia coli str. K-12 substr. MG1655
PROVIDER: GSE54902 | GEO | 2023/01/05
REPOSITORIES: GEO
Similar Datasets
Project description:NtrC and Nac have been known to be responsible for responding to nitrogen limitting conditions. In order to elucidate NtrC and Nac regulons in a genome-wide manner, RNA-seq and ChIP-exo experiments were performed for those two transcription factors under 4 different nitrogen sources, ammonia, glutamine, cytidine and cytosine.
2023-01-05 | GSE54904 | 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 | 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:We show that NtrC couples the Ntr stress response and stringent response in N starved E. coli, which appears to be a conserved adaptive strategy employed by many bacteria to manage conditions of nutritional adversity. N starved Escherichia coli initiate the nitrogen regulation (Ntr) stress response as an adaptive mechanism to scavenge for alternative N sources. The Ntr stress response requires the global transcriptional regulator nitrogen regulatory protein C (NtrC). We discovered that the transcription of relA, the key gene responsible for the synthesis of the major effector nucleotide alamorne of the bacterial stringent response, guanosine pentaphosphate (ppGpp), is positively regulated by NtrC in N starved E. coli. we addressed Ntr stress response-ppGpp alarmone links and mapped the genome-wide binding targets of NtrC in E. coli during N starvation using chromatin immunoprecipitation (ChIP) followed by high-throughput sequencing (ChIP-seq) to gain insight into the NtrC-dependent gene networks. To identify candidate genome regions that are preferentially associated with NtrC, we introduced an in-frame fusion encoding three repeats of the FLAG epitope to the 3-prime end of glnG in E. coli strain NCM3722, a prototrophic E. coli K-12 strain.
2014-05-01 | E-MTAB-2211 | biostudies-arrayexpress
Project description:Azospirillum brasilense is a free-living diazothophic bacterium that associates with important grasses and cereals, promoting plant growth and increasing crop productivity. The nitrogen metabolism in this organism is tightly regulated by the availability of nitrogen and by the Ntr regulatory system. This system comprises the GlnD protein, which is capable of adding uridylyl groups to the PII proteins, GlnB and GlnZ, under limiting nitrogen levels. Under such conditions, the histidine kinase NtrB cannot interact with GlnB and phosphorylate NtrC. When phosphorylated, NtrC is a transcriptional activator of genes involved in metabolism of alternative nitrogen sources. Considering the key role of NtrC in nitrogen metabolism in Azospirillum brasilense, in this work we evaluated the proteomic and metabolomic profiles of the wild type FP2 strain and its mutant ntrC grown under high and low nitrogen. Analysis of the integrated data identifies, novel NtrC targets, including proteins involved in the response against oxidative stressnm (i.e., glutathione S-transferase and hydroperoxide resistance protein,), underlining the importance of NtrC to bacterial survival under oxidative stress conditions.
2019-10-14 | PXD014120 | Pride
Project description:Here we demonstrate by experimental evolution and genetics the rapid and repeatable evolutionary re-wiring of regulatory pathways, where the cellular nitrogen regulatory system acquired the ability to “cross-talk” with the flagellar regulon. This rewiring restored flagella to aflagellate strains of Pseudomonas fluorescens devoid of the master regulator fleQ via a repeatable two-step evolutionary pathway. Step 1 initiates cross-talk by increasing intracellular levels of phosphorylated NtrC , a distant homologue of FleQ, which begins to commandeer control of the fleQ regulon whilst constitutively activating nitrogen uptake and assimilation genes. Step 2 is a switch-of-function mutation (NtrC’) that further redirects NtrC towards activation of motility and away from nitrogen uptake. Evolved NtrC’ emerges with a novel function as a flagellar regulator. Our results demonstrate that natural selection can rapidly rewire regulatory networks in very few, repeatable mutational steps to adopt new functionality.
2015-07-04 | E-MTAB-2788 | biostudies-arrayexpress
Project description:Assimilation of nitrogen is an essential process in bacteria. The nitrogen regulation stress response is an adaptive mechanism used by nitrogen-starved Escherichia coli to scavenge for alternative nitrogen sources and requires the global transcriptional regulator NtrC.
2014-06-17 | E-MTAB-2612 | biostudies-arrayexpress
Project description:H. seropedicae wild-type or ntrC mutant were grown on three different nitrogen conditions: nitrogen limiting, ammonium shock and nitrate shock.
2024-07-02 | E-MTAB-8238 | biostudies-arrayexpress
Project description:The Bradyrhizobium japonicum NtrC regulatory protein influences gene expression in response to changes in intracellular nitrogen status. Under conditions of low nitrogen, phosphorylation of NtrC results in up-regulation of a number of genes involved in nitrogen metabolism and nitrogen acquisition. To better define the exact nature of NtrC’s influence on gene expression, a ntrC mutation was created in B. japonicum and transcriptional profiling was performed by DNA microarray analysis of both the mutant and wild type strains.
2012-07-01 | GSE23870 | GEO
Project description:The Bradyrhizobium japonicum NtrC regulatory protein influences gene expression in response to changes in intracellular nitrogen status. Under conditions of low nitrogen, phosphorylation of NtrC results in up-regulation of a number of genes involved in nitrogen metabolism and nitrogen acquisition. To better define the exact nature of NtrC’s influence on gene expression, a ntrC mutation was created in B. japonicum and transcriptional profiling was performed by DNA microarray analysis of both the mutant and wild type strains.
2015-06-25 | GSE66091 | GEO