Widespread prevalence of a post-translational modification in activation of an essential bacterial DNA damage response (ChIP-seq)
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ABSTRACT:
PROVIDER: PRJNA1032077 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26521183.fastq.gz | Fastqsanger.gz | |||
| SRR26521184.fastq.gz | Fastqsanger.gz | |||
| SRR26521185.fastq.gz | Fastqsanger.gz | |||
| SRR26521186.fastq.gz | Fastqsanger.gz | |||
| SRR26521187.fastq.gz | Fastqsanger.gz |
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Project description:DNA methylation plays central roles in diverse cellular processes, ranging from error-correction during replication to regulation of bacterial defense mechanisms. Nevertheless, certain aberrant methylation modifications can have lethal consequences. The mechanisms by which bacteria detect and respond to such damage remain incompletely understood. Here, we discover a highly conserved but previously uncharacterized transcription factor (Cada2), which orchestrates a methylation-dependent adaptive response inCaulobacter. This response operates independently of the SOS response, governs the expression of genes crucial for direct repair, and is essential for surviving methylation-induced damage. Our molecular investigation of Cada2 reveals a cysteine methylation-dependent post-translational modification and mode of action distinct from itsE. colicounterpart, a trait conserved across all bacteria harboring a Cada2-like homolog instead. Extending across the bacterial kingdom, our findings support the notion of divergence and co-evolution of adaptive response transcription factors and their corresponding sequence-specific DNA motifs. Despite this diversity, the ubiquitous prevalence of adaptive response regulators underscores the significance of a transcriptional switch, mediated by methylation post-translational modification, in driving a specific and essential bacterial DNA damage response.
2024-02-01 | GSE246227 | GEO
Project description:DNA methylation plays central roles in diverse cellular processes, ranging from error-correction during replication to regulation of bacterial defense mechanisms. Nevertheless, certain aberrant methylation modifications can have lethal consequences. The mechanisms by which bacteria detect and respond to such damage remain incompletely understood. Here, we discover a highly conserved but previously uncharacterized transcription factor (Cada2), which orchestrates a methylation-dependent adaptive response inCaulobacter. This response operates independently of the SOS response, governs the expression of genes crucial for direct repair, and is essential for surviving methylation-induced damage. Our molecular investigation of Cada2 reveals a cysteine methylation-dependent post-translational modification and mode of action distinct from itsE. colicounterpart, a trait conserved across all bacteria harboring a Cada2-like homolog instead. Extending across the bacterial kingdom, our findings support the notion of divergence and co-evolution of adaptive response transcription factors and their corresponding sequence-specific DNA motifs. Despite this diversity, the ubiquitous prevalence of adaptive response regulators underscores the significance of a transcriptional switch, mediated by methylation post-translational modification, in driving a specific and essential bacterial DNA damage response.
2024-02-01 | GSE246782 | GEO
Project description:Widespread prevalence of a post-translational modification in activation of an essential bacterial DNA damage response (RNA-seq)
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Project description:DNA methylation plays central roles in diverse cellular processes, ranging from error-correction during replication to regulation of bacterial defense mechanisms. Nevertheless, certain aberrant methylation modifications can have lethal consequences. The mechanisms by which bacteria detect and respond to such damage remain incompletely understood. Here, we discover a highly conserved but previously uncharacterized transcription factor (Cada2), which orchestrates a methylation-dependent adaptive response in Caulobacter. This response operates independently of the SOS response, governs the expression of genes crucial for direct repair, and is essential for surviving methylation-induced damage. Our molecular investigation of Cada2 reveals a cysteine methylation-dependent post-translational modification and mode of action distinct from its E. coli counterpart, a trait conserved across all bacteria harboring a Cada2-like homolog instead. Extending across the bacterial kingdom, our findings support the notion of divergence and co-evolution of adaptive response transcription factors and their corresponding sequence-specific DNA motifs. Despite this diversity, the ubiquitous prevalence of adaptive response regulators underscores the significance of a transcriptional switch, mediated by methylation post-translational modification, in driving a specific and essential bacterial DNA damage response.
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Project description:This dataset compares the proteomes of WT P. fluorescens and a delta-hfq mutant strain. This forms part of our characterisation of a new mechanism for translational control in bacteria, based on the covalent modification of a ribosomal protein by the enzyme RimK. RimK modification induces specific effects on ribosomal stability and function, which in turn affects the abundance of the important translational regulator Hfq. RimK is itself controlled by binding to the small regulatory proteins RimA and RimB and the widespread signalling molecule cyclic-di-GMP. Deletion of rimK compromises motility, virulence and plant colonisation/infection in several different Pseudomonas species. Changes in intracellular RimK activity enable Pseudomonas to translate environmental pressures into dynamic ribosomal changes, and in turn into adaptive phenotypic responses to the surroundings. This promotes motility and virulence during the initial stages of plant contact, and phenotypes including attachment, metabolite transport and stress control during long-term environmental adaptation.
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2015-06-04 | E-GEOD-63120 | biostudies-arrayexpress
Project description:Cell development requires tight yet dynamic control of protein production. Here, we use murine erythropoiesis as a model to study translational regulatory dynamics during mammalian cell differentiation. We uncover pervasive translational control of protein synthesis, including widespread alternative translation initiation and termination, stoichiometric synthesis, and dynamic use of upstream reading frames. We thus unravel translational regulatory programs during erythropoiesis, comprising hundreds of mRNAs with dynamic translation efficiencies and their cell type-specific regulators. A major such program involves enhanced decoding of specific mRNAs depleted in terminally differentiating/enucleating cells with decreasing transcriptional capacity. Rbm38, an erythroid-specific RNA-binding protein, promotes translation of many such genes by recruiting the translation initiation factor eIF4G. Inhibiting Rbm38 blocks red cell production, and mice lacking Rbm38 develop anemia, demonstrating an essential role for Rbm38-mediated enhanced translation of irreplaceable mRNAs. These findings reveal critical roles for dynamic translational control in supporting specialized mammalian cell formation.
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Project description:Post-transcriptional modifications are important for transfer RNAs (tRNAs) to be efficient and accurate in translation on the ribosome. The m1G37 modification on a subset of tRNAs in bacteria are generated by a conserved methyltransferase TrmD and is essential for bacterial growth. Previous studies showed that m1G37 has an important role in preventing translational frameshifting and also that this modification is coupled with aminoacylation of tRNAs for proline. Here we performed suppressor screening to isolate a mutant E. coli cell that lacks TrmD but is viable, and the whole-genome sequencing revealed several mutations on prolyl-tRNA synthetase (ProRS) gene conferring cell viability in the absence of TrmD. Biochemical assays confirmed uncoupling of m1G37 modification and aminoacylation, and cell-based assays uncovered the critical role of m1G37 in supporting Wobble decoding.
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