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Bacillus subtilis subsp. subtilis str. 168

ABSTRACT: Transcriptome analysis of glucose starved Bacillus subtilis cells

OTHER RELATED OMICS DATASETS IN: PXD000181

PROVIDER: PRJNA130141 | ENA |

REPOSITORIES: ENA

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Bacillus subtilis WalR (YycF) ChIP-chip Bacillus subtilis; Bacillus subtilis subsp. subtilis str. 168

2015-01-26 | GSE65272 | GEO

Bacillus subtilis WalR (YycF) ChIP-chip Bacillus subtilis; Bacillus subtilis subsp. subtilis str. 168

Project description:Identification of the specific WalR (YycF) binding regions on the B. subtilis chromosome during exponential and phosphate starvation growth phases. The data serves to extend the WalRK regulon in Bacillus subtilis and its role in cell wall metabolism, as well as implying a role in several other cellular processes. For each sample analyzed in this study three biological replicates were performed. Three different samples were taken from a strain expressing the WalR-SPA protein as well as from wild-type (168) without a tagged WalR. Samples were taken from exponentially growing cells in low phosphate medium (LPDM) as well as from phosphate-limited cells (T2). Each sample compares ChIP DNA vs. Total DNA from the same cells.

2015-01-26 | E-GEOD-65272 | biostudies-arrayexpress

Bacillus subtilis 168 moenomycin stimulon

Project description:Transcriptional response of Bacillus subtilis to moenomycin in wild-type 168.

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Project description:To explore the effects of different stress conditions on Bacillus subtilis str.168, a selection of conditions were applied to the organism and RNA-seq data gathered. A matrix of gene counts was produced as a basis for further analysis into the transcription profiles of Bacillus subtilis str.168.

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Bacillus subtilis 168 moenomycin stimulon

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Expression data from Bacillus subtilis 168 during growth

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Bacillus subtilis 168 cells: wild-type vs. ccpN (non polar)

Project description:Global transcriptional profiling of Bacillus subtilis cells comparing wild-type to a ccpN (yqzB) non polar mutant. Abstract of associated publication (article accepted): The transcriptional regulator CcpN of Bacillus subtilis has been recently characterized as a repressor of two gluconeogenic genes, gapB and pckA, and of a small non-coding regulatory RNA, sr1, involved in arginine catabolism. Deletion of ccpN impairs growth on glucose and strongly alters the distribution of intracellular fluxes, rerouting the main glucose catabolism from glycolysis to the pentose phosphate (PP) pathway. Using transcriptome analysis, we show that during growth on glucose, gapB and pckA are the only protein-coding genes directly repressed by CcpN. By quantifying intracellular fluxes in deletion mutants, we demonstrate that derepression of pckA under glycolytic condition causes the growth defect observed in the ccpN mutant due to extensive futile cycling through the pyruvate carboxylase, phosphoenolpyruvate carboxykinase, and pyruvate kinase. Beyond ATP dissipation via this cycle, PckA activity causes a drain on tricarboxylic acid cycle intermediates, which we show to be the main reason for the reduced growth of a ccpN mutant. The high flux through the PP pathway in the ccpN mutant is modulated by the flux through the alternative glyceraldehyde-3-phosphate dehydrogenases, GapA and GapB. Strongly increased concentrations of intermediates in upper glycolysis indicate that GapB overexpression causes a metabolic jamming of this pathway and, consequently, increases the relative flux through the PP pathway. In contrast, derepression of sr1, the third known target of CcpN, plays only a marginal role in ccpN mutant phenotypes.

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