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Widespread prevalence of a post-translational modification in activation of an essential bacterial DNA damage response (RNA-seq)

ABSTRACT: Widespread prevalence of a post-translational modification in activation of an essential bacterial DNA damage response (RNA-seq)

PROVIDER: PRJNA1034607 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26629018_1.fastq.gz	Fastqsanger.gz
	SRR26629018_2.fastq.gz	Fastqsanger.gz
	SRR26629019_1.fastq.gz	Fastqsanger.gz
	SRR26629019_2.fastq.gz	Fastqsanger.gz
	SRR26629020_1.fastq.gz	Fastqsanger.gz

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Widespread prevalence of a post-translational modification in activation of an essential bacterial DNA damage response (RNA-seq)

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

Widespread prevalence of a post-translational modification in activation of an essential bacterial DNA damage response (ChIP-seq)

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Widespread prevalence of a post-translational modification in activation of an essential bacterial DNA damage response (ChIP-seq)

Project description:Widespread prevalence of a post-translational modification in activation of an essential bacterial DNA damage response (ChIP-seq)

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Widespread prevalence of a post-translational modification in activation of an essential bacterial DNA damage response

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.

2024-02-09 | PXD049136 | Pride

Post-translational Modification of RNA m6A Demethylase ALKBH5 Regulates ROS-induced DNA Damage Response

Project description:Post-translational Modification of RNA m6A Demethylase ALKBH5 Regulates ROS-induced DNA Damage Response

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Widespread Co-translational RNA Decay Reveals Ribosome Dynamics

Project description:Widespread Co-translational RNA Decay Reveals Ribosome Dynamics

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Role of eEF2 diphthamide modification in translational fidelity

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Translational regulation via ribosome modification

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.

2016-02-17 | PXD002573 | Pride

Widespread Co-translational RNA Decay Reveals Ribosome Dynamics

Project description:It is generally assumed that mRNAs undergoing translation are protected from decay. Here, we show that mRNAs are, in fact, co-translationally degraded. This is a widespread and conserved process affecting most genes, where 5′–3′ transcript degradation follows the last translating ribosome, producing an in vivo ribosomal footprint. By sequencing the ends of 5′ phosphorylated mRNA degradation intermediates, we obtain a genome-wide drug-free measurement of ribosome dynamics. We identify general translation termination pauses in both normal and stress conditions. In addition, we describe novel codon-specific ribosomal pausing sites in response to oxidative stress that are dependent on the RNase Rny1. Our approach is simple and straightforward and does not require the use of translational inhibitors or in vitro RNA footprinting that can alter ribosome protection patterns. RNA samples were quantified according to their 5’modification. Samples were quantified using 2 alternative methods. 5PSeq (measures 5’P RNAs) and 5PSeq-fragmented (measures the sequencing bias present in any sample by randomly fragmenting RNA, re-phosphorilating the 5’ends and subjecting the sample to 5PSeq; it is used as a negative control). Different strains of S. cerevisiae and S. pombe samples were analyzed. Cells were grown both in rich media (YPD or YES) and synthetic defined media (SD). Cells were subjected to different treatments such as inhibition of translation elongation with cyclohexamide (CHX), oxidative stress (0.2 mM H2O2) or inhibition of histidine biosyntesys (3-AT; 100mM 3-amino-1,2,4-triazole). S. cerevisiae samples grown in rich media were also analyzed after CHX treatment and sucrose fractionation into monosome and polyribosome fractionation. All samples were analyzed in biological duplicates.

2015-06-04 | E-GEOD-63120 | biostudies-arrayexpress

ROSALIND protects the mitochondrial translational machinery from oxidative damage

Project description:ROSALIND protects the mitochondrial translational machinery from oxidative damage

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