Heat shock induces silent ribosomes and reorganizes mRNA turnover
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ABSTRACT:
PROVIDER: PRJNA1223295 | ENA |
REPOSITORIES: ENA
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Project description:mRNAs associate with single or multiple ribosomes; these ribosomal assemblies —monosomes and polysomes — translate the mRNAs before degradation. The impact of heat stress on this mRNA turnover remains unclear. In heat-shocked yeast cells, the proportion of monosomes within the ribosomal assemblies rises without a corresponding increase in the number of mRNAs associated with them. As a result, most monosomes are devoid of mRNAs and silent, lacking translational initiation factors and proteins facilitating posttranslational folding. The accumulation of silent ribosomes generally reduces the rate of association of transcripts with the ribosomes. However, elevated temperatures enhance the ribosomal association of specific mRNAs, primarily those encoding heat-shock proteins, allowing them to balance their increased degradation rates. Additionally, reduced binding of the Xrn1 exonuclease to mRNAs diminishes the influence of codon optimality on mRNA stability. These mechanisms reconfigure the translation machinery to prioritize heat-shock protein synthesis over ribosome biogenesis.
2025-09-10 | GSE289484 | GEO
Project description:mRNAs associate with single or multiple ribosomes these ribosomal assemblies monosomes and polysomes translate the mRNAs before degradation. The impact of heat stress on this mRNA turnover remains unclear. We show that in heat-shocked yeast cells, the proportion of monosomes increases without a corresponding rise in the number of associated mRNAs. Consequently, most monosomes are devoid of mRNAs and silent, lacking translational initiation factors and proteins facilitating posttranslational folding. Such silent monosomes also appear under other stress conditions, with proportions varying according to stress type, suggesting they represent a general feature of cellular adaptation. In parallel with the induction of silent ribosomes, elevated temperatures reduce the overall rate of mRNA ribosome association with few exceptions. Notably, heat-shock promotes the ribosomal association of transcripts encoding heatshock proteins, without extension of the halflives of these mRNAs. These mechanisms dynamically reorganize mRNA turnover to prioritize translation of heat-shock proteins over other proteins.
| MSV000099165 | MassIVE
Project description:Cells can respond to stalled ribosomes by sensing ribosome collisions and employing quality control pathways. How ribosome stalling is resolved without collisions, however, has remained elusive. Here, focusing on non-colliding stalling exhibited by decoding-defective ribosomes, we identified Fap1 as a stalling sensor triggering 18S non-functional rRNA decay via poly-ubiquitination of uS3. Ribosome profiling revealed an enrichment of Fap1 at the translation initiation site but also association with elongating individual ribosomes. Cryo-EM structures of Fap1-bound ribosomes elucidated Fap1 probing the mRNA simultaneously at both the entry and exit channels suggesting a mRNA stasis sensing activity, and Fap1 sterically hinders formation of canonical collided di-ribosomes. Our findings indicate that individual stalled ribosomes are the potential signal for ribosome dysfunction, leading to accelerated turnover of the ribosome itself.
2022-09-15 | GSE159329 | GEO
Project description:Heat shock rapidly induces expression of a small set of genes while globally repressing transcription, making it an attractive system for studying alterations in the chromatin landscape that accompany changes in gene regulation. We have characterized these changes using low-salt extraction of intact micrococcal nuclease (MNase)-treated Drosophila S2 cell nuclei to determine the active nucleosomal and subnucleosomal chromatin landscapes. The low-salt-soluble fraction corresponds to classical "active" chromatin and includes distinct size fractions of MNase-protected particles that can be precisely mapped by paired-end sequencing. After heat shock, the distribution of low-salt-soluble nucleosomes showed an overall reduction over gene bodies, consistent with down-regulation of transcription. No global changes were detected in the subnucleosomal landscape upstream of transcriptional start sites, however, we observed a genome-wide reduction of paused RNA Polymerase II from the active chromatin fraction. Furthermore, nucleosome turnover decreased within gene bodies in a pattern similar to that observed when transcription elongation was artificially inhibited. These observations suggest that reduced Pol II affinity and processivity is the dominant nuclear mechanism for genome-wide repression during heat shock. Our ability to precisely map both nucleosomal and subnucleosomal particles directly from classical active chromatin extracts to assay changes in the chromatin landscape provides a simple general strategy for epigenome characterization. High-throughput sequencing (Illumina HiSeq 2000) We have characterized changes to the active nucleosomal and subnucleosomal landscape during the heat shock response in Drosophila cells by genome-wide profiling of low-salt extracted micrococcal nuclease-treated nuclei, paused RNA Polymerase II and CATCH-IT nucleosome turnover.
2011-11-15 | E-GEOD-30755 | biostudies-arrayexpress
Project description:Sensing of individual stalled 80S ribosomes by Fap1 for non-functional rRNA turnover. Li et al
| PRJNA668372 | ENA
Project description:Heat shock rapidly induces expression of a small set of genes while globally repressing transcription, making it an attractive system for studying alterations in the chromatin landscape that accompany changes in gene regulation. We have characterized these changes using low-salt extraction of intact micrococcal nuclease (MNase)-treated Drosophila S2 cell nuclei to determine the active nucleosomal and subnucleosomal chromatin landscapes. The low-salt-soluble fraction corresponds to classical "active" chromatin and includes distinct size fractions of MNase-protected particles that can be precisely mapped by paired-end sequencing. After heat shock, the distribution of low-salt-soluble nucleosomes showed an overall reduction over gene bodies, consistent with down-regulation of transcription. No global changes were detected in the subnucleosomal landscape upstream of transcriptional start sites, however, we observed a genome-wide reduction of paused RNA Polymerase II from the active chromatin fraction. Furthermore, nucleosome turnover decreased within gene bodies in a pattern similar to that observed when transcription elongation was artificially inhibited. These observations suggest that reduced Pol II affinity and processivity is the dominant nuclear mechanism for genome-wide repression during heat shock. Our ability to precisely map both nucleosomal and subnucleosomal particles directly from classical active chromatin extracts to assay changes in the chromatin landscape provides a simple general strategy for epigenome characterization.
2011-11-15 | GSE30755 | GEO
Project description:Flagellins from commensal bacteria can be weak Toll-like receptor (TLR)5 agonists despite high affinity binding to TLR5, ligands we termed “silent flagellins”. To determine if silent flagellins are detectable in the human gut, endogenous flagellins produced by the microbiota were isolated from stool obtained from a healthy adult female donor. TLR5 was used as bait to enrich for silent flagellins and TLR5-bound flagellins were identified by searching peptides against a custom flagellin database built from metagenome sequences.
2022-10-12 | PXD033249 | Pride
Project description:A total of 10 cDNA libraries were constructed, representing 3 and 2 independent biological replicates of S. aureus strain KES34 (unmodified ribosomes) and KES30 (m6A2058-modified ribosomes), respectively. Translational efficiency (RPF/mRNA ratios), total mRNA abundance and ribosome density of each ORFs were calculated.
2024-01-16 | GSE168265 | GEO
Project description:Silent nociceptors are sensory afferents that are insensitive to noxious mechanical stimuli under normal conditions but become sensitized to such stimuli during inflammation. We had previously shown that mouse silent nociceptors express the nicotinic acetylcholine receptor alpha-3 subunit (CHRNA3) and can thus readily be identified in Tg(Chrna3-EGFP)BZ135Gsat reporter mice (Prato et al. Cell Reports 2017). Most importantly, we had shown that CHRNA3+ slient nociceptors acquire mechanosensitivity upon treatment with the inflammatory mediator nerve growth factor and demonstrated that this process requires de-novo gene transcription. Here, we performed paired-end RNA-sequencing to identify transcripts that might be involved in the acquisition of mechanosenstivity in mouse silent nociceptors.
2022-12-01 | GSE199580 | GEO
Project description:NGF-induced gene expression in silent nociceptors
| PRJNA820757 | ENA