A stress response that monitors and regulates mRNA structure is central to cold-shock adaptation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA401857 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6001740.fastq.gz | Fastqsanger.gz | |||
| SRR6001750.fastq.gz | Fastqsanger.gz | |||
| SRR6001760.fastq.gz | Fastqsanger.gz | |||
| SRR6001770.fastq.gz | Fastqsanger.gz | |||
| SRR6001780.fastq.gz | Fastqsanger.gz |
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Project description:Temperature influences the structural and functional properties of cellular components, necessitating stress responses to restore homeostasis following temperature shift. The heat shock circuitry is well understood, but that controlling the E. coli cold-shock adaptation program is not. We found that during the growth arrest phase (acclimation) that follows shift to low temperature, protein synthesis increases and ORF-wide mRNA secondary structure decreases. We identified two components of an mRNA surveillance system that enable recovery of translation during acclimation: RNase R assures appropriate mRNA degradation and the Csps dynamically adjust mRNA secondary structure to globally modulate protein expression level. Csps also remodel their own mRNAs to tune their expression to cellular need. Thus, appropriate translation is dynamically adjusted with Csp control. The universality of Csps in bacteria suggests broad utilization of this control mechanism.
2018-04-21 | GSE103421 | GEO
Project description:Temperature influences the structural and functional properties of cellular components, necessitating stress responses to restore homeostasis following temperature shift. Whereas the circuitry controlling the heat shock response is well understood, that controlling the E. coli cold shock adaptation program is not. We found that during the growth arrest phase (acclimation) that follows shift to low temperature, protein synthesis increases, and open reading frame (ORF)-wide mRNA secondary structure decreases. To identify the regulatory system controlling this process, we screened for players required for increased translation. We identified a two-member mRNA surveillance system that enables recovery of translation during acclimation: RNase R assures appropriate mRNA degradation and the Csps dynamically adjust mRNA secondary structure to globally modulate protein expression level. An autoregulatory switch in which Csps tune their own expression to cellular demand enables dynamic control of global translation. The universality of Csps in bacteria suggests broad utilization of this control mechanism.
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Project description:The ability to rapidly respond to changes in temperature is critical for insects and other ectotherms living in variable environments. In a physiological process termed rapid cold-hardening (RCH), exposure to non-lethal low temperature allows many insects to significantly increase their cold tolerance in a matter of minutes to hours. Additionally, there are rapid changes in gene expression and cell physiology during recovery from cold injury, and we hypothesize that RCH may modulate some of these processes during recovery. In this study, we used a cDNA microarray to examine the molecular mechanisms of RCH and cold shock (CS) recovery in the flesh fly, Sarcophaga bullata. With our custom 2-color array, we measured expression of ~15,000 ESTs during RCH and during recovery from cold shock. Surprisingly, no transcripts were upregulated during RCH, and likewise, RCH had a minimal effect on the transcript signature during recovery from cold shock. However, during recovery from cold shock, we observed differential expression of ~1,400 ESTs, including a number of heat shock proteins, cytoskeletal components, and genes from several cell signaling pathways. Several gene pathways correlated well with metabolomics data, indicating that coordinated changes in gene expression and metabolism contribute to recovery from cold shock.
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Project description:Profound understanding of the mechanisms foodborne pathogenic bacteria utilize in adaptation to the environmental stress they encounter during food processing and storage is of paramount importance in design of control measures. Chill temperature is a central control measure applied in minimally processed foods; however, data on the mechanisms the foodborne pathogen Clostridium botulinum activates upon cold stress are scarce. Global gene expression analysis on the C.M-BM- botulinum ATCC 3502 strain upon temperature downshift from 37 M-BM-0C to 15M-BM- M-BM-0C was performed to identify the cold-responsive gene set of this organism. Significant up- or down-regulation of 16 and 11 genes, respectively, was observed already 1 h after the cold shock. At 5 h after the temperature downshift, 199 and 210 genes were up- and down-regulated, respectively. Thus, the cold shock rapidly affected the expression of a gene set of a relatively small size, indicating a targeted acute response to cold shock, whereas extensive metabolic remodeling took place after prolonged exposure to cold. Induction of genes related to fatty acid biosynthesis, oxidative stress response, and iron uptake and storage was observed, in addition to mechanisms previously characterized as cold-tolerance related in bacteria. Furthermore, induction of several uncharacterized DNA-binding transcriptional regulator-encoding genes was observed, suggesting involvement of novel regulatory mechanisms in the cold shock response of C.M-BM- botulinum. The role of such regulatory proteins, CBO0477 and CBO0558A, in cold tolerance of C.M-BM- botulinum ATCC 3502 was demonstrated by the deteriorated growth of mutants of the respective genes at 17M-BM- M-BM-0C. C. botulinum ATCC 3502 wild type cold-shocked vs. pre-cold-shock; 3 replicates; growth at 37C in TPGY broth batch culture and subjected to cold shock to 15C; sampling at mid-log growth phase before cold shock, and 1 h and 5 h after temperature downshift to 15C (= 3 time points). Dye-swapped hybridization.
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Project description:Profound understanding of the mechanisms foodborne pathogenic bacteria utilize in adaptation to the environmental stress they encounter during food processing and storage is of paramount importance in design of control measures. Chill temperature is a central control measure applied in minimally processed foods; however, data on the mechanisms the foodborne pathogen Clostridium botulinum activates upon cold stress are scarce. Global gene expression analysis on the C. botulinum ATCC 3502 strain upon temperature downshift from 37 °C to 15 °C was performed to identify the cold-responsive gene set of this organism. Significant up- or down-regulation of 16 and 11 genes, respectively, was observed already 1 h after the cold shock. At 5 h after the temperature downshift, 199 and 210 genes were up- and down-regulated, respectively. Thus, the cold shock rapidly affected the expression of a gene set of a relatively small size, indicating a targeted acute response to cold shock, whereas extensive metabolic remodeling took place after prolonged exposure to cold. Induction of genes related to fatty acid biosynthesis, oxidative stress response, and iron uptake and storage was observed, in addition to mechanisms previously characterized as cold-tolerance related in bacteria. Furthermore, induction of several uncharacterized DNA-binding transcriptional regulator-encoding genes was observed, suggesting involvement of novel regulatory mechanisms in the cold shock response of C. botulinum. The role of such regulatory proteins, CBO0477 and CBO0558A, in cold tolerance of C. botulinum ATCC 3502 was demonstrated by the deteriorated growth of mutants of the respective genes at 17 °C.
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Project description:The ability to rapidly respond to changes in temperature is critical for insects and other ectotherms living in variable environments. In a physiological process termed rapid cold-hardening (RCH), exposure to non-lethal low temperature allows many insects to significantly increase their cold tolerance in a matter of minutes to hours. Additionally, there are rapid changes in gene expression and cell physiology during recovery from cold injury, and we hypothesize that RCH may modulate some of these processes during recovery. In this study, we used a cDNA microarray to examine the molecular mechanisms of RCH and cold shock (CS) recovery in the flesh fly, Sarcophaga bullata. With our custom 2-color array, we measured expression of ~15,000 ESTs during RCH and during recovery from cold shock. Surprisingly, no transcripts were upregulated during RCH, and likewise, RCH had a minimal effect on the transcript signature during recovery from cold shock. However, during recovery from cold shock, we observed differential expression of ~1,400 ESTs, including a number of heat shock proteins, cytoskeletal components, and genes from several cell signaling pathways. Several gene pathways correlated well with metabolomics data, indicating that coordinated changes in gene expression and metabolism contribute to recovery from cold shock. Four treatment groups (C, RCH, CS+2R, RCH+CS+2R), four biological replicates of four pooled individuals for each treatment. Each phenotype was hybridized with the control, and the CS+2R and RCH+CS+2R groups were also hybridized together.
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