Regulation of the transcription factor CdnL promotes adaptation to nutrient stress in Caulobacter
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1047613 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27019100.fastq.gz | Fastqsanger.gz | |||
| SRR27019101.fastq.gz | Fastqsanger.gz | |||
| SRR27019102.fastq.gz | Fastqsanger.gz | |||
| SRR27019094.fastq.gz | Fastqsanger.gz | |||
| SRR27019095.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 9 |
Similar Datasets
Project description:In response to nutrient deprivation, bacteria activate a conserved stress response pathway called the stringent response (SR). In Caulobacter crescentus, SpoT synthesizes the secondary messengers (p)ppGpp, which affect transcriptional reprogramming by binding to RNA polymerase to downregulate anabolic gene transcription. (p)ppGpp can also impact the expression of anabolic genes by controlling the levels and activities of their transcriptional regulators. In Caulobacter, a major regulator of anabolic genes is the conserved transcription factor CdnL. If and how CdnL is controlled during the SR and why that might be functionally important is unclear. Here, we show that CdnL is regulated post-translationally in a manner dependent on SpoT and the ClpXP protease. We find that stabilization of CdnL causes misregulation of ribosomal and metabolic genes during starvation. Functionally, we demonstrate that the combined action of SR transcriptional regulators and CdnL clearance allows for rapid adaptation to nutrient repletion. We also find that cells that are unable to clear CdnL during starvation are outcompeted by wild-type cells when subjected to fluctuations in nutrients. We hypothesize that post-transcriptional clearance of CdnL during the SR, in conjunction with direct binding of (p)ppGpp and DksA to RNAP, are critical for altering the transcriptome in order to permit cell survival during nutrient stress.
2024-05-10 | GSE249185 | GEO
Project description:In response to nutrient deprivation, bacteria activate a conserved stress response pathway called the stringent response (SR). During SR activation in Caulobacter crescentus, SpoT synthesizes the secondary messengers (p)ppGpp, which affect transcription by binding RNA polymerase to downregulate anabolic genes. (p)ppGpp also impacts expression of anabolic genes by controlling the levels and activities of their transcriptional regulators. In Caulobacter, a major regulator of anabolic genes is the transcription factor CdnL. If and how CdnL is controlled during the SR and why that might be functionally important is unclear. Here, we show that CdnL is downregulated post-translationally during starvation in a manner dependent on SpoT and the ClpXP protease. Inappropriate stabilization of CdnL during starvation causes misregulation of ribosomal and metabolic genes. Functionally, we demonstrate that the combined action of SR transcriptional regulators and CdnL clearance allows for rapid adaptation to nutrient repletion. Moreover, cells that are unable to clear CdnL during starvation are outcompeted by wild-type cells when subjected to nutrient fluctuations. We hypothesize that clearance of CdnL during the SR, in conjunction with direct binding of (p)ppGpp and DksA to RNAP, is critical for altering the transcriptome in order to permit cell survival during nutrient stress.
| S-EPMC10769358 | biostudies-literature
Project description:Start codon-associated ribosomal frameshifting mediates nutrient stress adaptation
| PRJNA766610 | ENA
Project description:Investigation of whole genome gene expression level changes in a Caulobacter crescentus NA1000 delta-CCNA_00382 (ccrM) mutant, compared to the wild-type strain. The mutations engineered into this strain render it incapable of methylating its genome on the adenine at GANTC motifs. References for strains : WT: Marks, M.E., Castro-Rojas, C.M., Teiling, C., Du, L., Kapatral, V., Walunas, T.L. and Crosson, S. (2010) The genetic basis of laboratory adaptation in Caulobacter crescentus. J Bacteriol, 192, 3678-3688; Collier, J. and Shapiro, L. (2009) Feedback control of DnaA-mediated replication initiation by replisome-associated HdaA protein in Caulobacter. J Bacteriol, 191, 5706-5716. DccrM: Gonzalez, D. and Collier, J. (2013) DNA methylation by CcrM activates the transcription of two genes required for the division of Caulobacter crescentus. Mol Microbiol, 88, 203-218. A six chip study using total RNA recovered from three separate wild-type cultures of Caulobacter crescentus NA1000 and three separate cultures of a triple mutant strain, Caulobacter crescentus NA1000 delta-CCNA_00382 (ccrM), in which the ccrM gene coding for a DNA methyltransferase methylating the adenine in GANTC motifs is truncated and its product inactive. Each chip measures the expression level of 3933 genes from Caulobacter crescentus NA1000 with 3 probes per gene and with three-fold technical redundancy.
2014-01-08 | E-GEOD-52375 | biostudies-arrayexpress
Project description:The mechanism of evolution in different conditions can be examined from various molecular aspects that constitute a cell, namely, transcript, protein or metabolite abundance. We have analyzed transcript and metabolite abundance changes in evolved and ancestor strains in three different evolutionary conditions, namely, excess-nutrient adaptation, prolonged stationary phase adaptation and adaptation due to environmental shift, in two different strains of Escherichia coli K-12 (MG1655 and DH10B).
2007-10-02 | E-MEXP-1166 | biostudies-arrayexpress
Project description:A translating ribosome is typically thought to follow the reading frame defined by the selected start codon. Using super-resolution ribosome profiling, here we report pervasive out-of-frame translation from the start codon. Unlike programmable frameshifting during elongation, start codon-associated ribosome frameshifting (SCARF) stems from the slippage of the initiating ribosome. Using a massively paralleled reporter assay, we uncovered sequence elements acting as SCARF enhancers or repressors, implying that start codon recognition is coupled with reading frame fidelity. This finding explains thousands of mass spectrometry spectra unannotated from human proteome. Mechanistically, we find that the eukaryotic initiation factor 5B (eIF5B) maintains the reading frame fidelity during the transition from initiation to elongation. Intriguingly, amino acid starvation induces SCARF by proteasomal degradation of eIF5B. The stress-induced SCARF products provide a degradative source to mitigate amino acid scarcity during starvation. Our findings illustrate the beneficial effect of divergent translation in nutrient stress adaptation.
2023-03-01 | GSE184825 | GEO
Project description:Investigation of whole genome gene expression level changes in a Caulonacter crescentus NA1000 Plac::CCNA_00382 (ccrM) mutant, compared to the wild-type strain. The mutations engineered into this strain cause the CcrM DNA methyltransferase to be overexpressed and the chromosome to be constitutively methylated at the adenine at GANTC motifs. References of strains: CcrMOE: Collier, J. and Shapiro, L. (2009) Feedback control of DnaA-mediated replication initiation by replisome-associated HdaA protein in Caulobacter. J Bacteriol, 191, 5706-5716. WT: Marks, M.E., Castro-Rojas, C.M., Teiling, C., Du, L., Kapatral, V., Walunas, T.L. and Crosson, S. (2010) The genetic basis of laboratory adaptation in Caulobacter crescentus. J Bacteriol, 192, 3678-3688; Collier, J. and Shapiro, L. (2009) Feedback control of DnaA-mediated replication initiation by replisome-associated HdaA protein in Caulobacter. J Bacteriol, 191, 5706-5716. A six chip study using total RNA recovered from three separate wild-type cultures of Caulonacter crescentus NA1000 and three separate cultures of a triple mutant strain, Caulonacter crescentus NA1000 Plac::CCNA_00382 (ccrM), in which the ccrM gene coding for a DNA methyltransferase methylating the adenine in GANTC motifs is truncated and its product inactive. Each chip measures the expression level of 3933 genes from Caulobacter crescentus NA1000 with 3 probes per gene and with three-fold technical redundancy.
2014-01-08 | E-GEOD-52722 | biostudies-arrayexpress
Project description:Investigation of whole genome gene expression level changes in a Caulobacter crescentus NA1000 delta-CCNA_00382 (ccrM) mutant, compared to the wild-type strain. The mutations engineered into this strain render it incapable of methylating its genome on the adenine at GANTC motifs. References for strains : WT: Marks, M.E., Castro-Rojas, C.M., Teiling, C., Du, L., Kapatral, V., Walunas, T.L. and Crosson, S. (2010) The genetic basis of laboratory adaptation in Caulobacter crescentus. J Bacteriol, 192, 3678-3688; Collier, J. and Shapiro, L. (2009) Feedback control of DnaA-mediated replication initiation by replisome-associated HdaA protein in Caulobacter. J Bacteriol, 191, 5706-5716. DccrM: Gonzalez, D. and Collier, J. (2013) DNA methylation by CcrM activates the transcription of two genes required for the division of Caulobacter crescentus. Mol Microbiol, 88, 203-218.
2014-01-08 | GSE52375 | GEO
Project description:Investigation of whole genome gene expression level changes in a Caulonacter crescentus NA1000 Plac::CCNA_00382 (ccrM) mutant, compared to the wild-type strain. The mutations engineered into this strain cause the CcrM DNA methyltransferase to be overexpressed and the chromosome to be constitutively methylated at the adenine at GANTC motifs. References of strains: CcrMOE: Collier, J. and Shapiro, L. (2009) Feedback control of DnaA-mediated replication initiation by replisome-associated HdaA protein in Caulobacter. J Bacteriol, 191, 5706-5716. WT: Marks, M.E., Castro-Rojas, C.M., Teiling, C., Du, L., Kapatral, V., Walunas, T.L. and Crosson, S. (2010) The genetic basis of laboratory adaptation in Caulobacter crescentus. J Bacteriol, 192, 3678-3688; Collier, J. and Shapiro, L. (2009) Feedback control of DnaA-mediated replication initiation by replisome-associated HdaA protein in Caulobacter. J Bacteriol, 191, 5706-5716.
2014-01-08 | GSE52722 | GEO
Project description:Candida glabrata is an important human fungal pathogen leading cause of non-albicans Candida infections. C. glabrata exhibits resistance to key antifungal drugs, rapidly replicates and divides in host macrophages and withstands highly stressful host conditions. This study explores the molecular mechanisms underlying stress adaptations in C. glabrata that contribute to its pathogenicity. Our findings revealed that C. glabrata survives oxidative stress and amino acid starvation more effectively than S. cerevisiae, C. albicans, and C. auris. We noted that Gcn2 kinase and Gcn4 play critical roles in this adaptation as Gcn2 phosphorylates eIF2α and downregulates the global protein translation, activating GCN4. RNA sequencing of WT and gcn4 mutant revealed that GCN4 activation during stress orchestrates the expression of stress-responsive genes vital for survival during amino acid starvation and oxidative stress. Ultimately assisting in the stress adaptative transcriptome. Thus, this study highlights the critical role of the Gcn2–Gcn4 pathway in stress adaptation in C. glabrata.
2025-07-14 | GSE283533 | GEO