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Neuronal ire-1 coordinates an organism-wide cold stress response by regulating fat metabolism - Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and ire-1(ok799) Transcriptomes During Cold Stress.

ABSTRACT: Cold affects many aspects of biology, medicine, agriculture and industry. Here, we identify a conserved endoplasmic reticulum (ER) stress response, distinct from the canonical unfolded protein response, which maintains lipid homeostasis during extreme cold stress. We establish that the ER stress sensor IRE-1 is critical for resistance to extreme cold and is activated by cold temperature. Specifically, neuronal IRE-1 signals via JNK-1 and neuropeptide-mediated signalling to regulate lipid composition throughout the animal. The requirement of this cold-response pathway can be bypassed by supplementation with unsaturated fatty acids or by altering the diet . Altogether, our findings define an ER-centric conserved organism-wide cold stress response pathway, consisting of sensors, effectors and signalling moieties, which control adaptation to cold throughout the organism. Better understanding of the molecular basis of cold adaptation is crucial for the design of safe and optimal use of cold conditions on live organisms and samples, and for the development of better treatments for hypothermia. Conclusions: Our study represents a detailed analysis of C.elegans transcriptomes during cold stress, with biological replicates, generated by RNA-seq technology.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE193923 | GEO | 2022/11/15

REPOSITORIES: GEO

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Project description:Stress leads to important adaptive physiological responses including release of catecholamines from the adrenal medulla. Repeated or prolonged stress increases the propensity for many disorders including cardiovascular disease and neuropsychiatric disorders. The susceptibility to stress is determined by a number of factors including prior experience with stress. It has been found that while there is adaptation to prolonged cold stress; it leads to sensitization when cold stressed animals are exposed to a different (novel) stressor. Our study aims to determine the mechanism of this adaptation and sensitization.,We will determine the gene expression patterns in rat adrenal medulla in response to several times of cold stress. We will also determine the changes in gene expression with single immobilization stress in adrenal medulla of rat with and without preexposure to cold stress to investigate the mechanism of sensitization in cold adapted animals. ,We hypothesize that during the course of cold stress there are alterations in gene expression of several neurotransmitter related genes and transcription factors. In cold adapted animals, there is increased susceptibility to stress due to sustained changes in expression of several transcription factors, such as FRA-2 which lead to an exaggerated response to the novel stressor. ,Rats were exposed to cold stress (4oC) for 1, 7 or 28 days. A parallel group was kept at room temperature (unstressed). Unstressed or rats pre-exposed to 28 days cold were immobilized for 2 hrs and killed by decapitation. The adrenal medullae, separately from right and left side, have been dissected and individually frozen at -70oC. Our recent immunoblots with the tissue from one side revealed that there is increase in tyrosine hydroxylase and c-fos with the short term cold stress and in dopamine beta hydroxylase and Fra-2 even with the prolonged cold stress. The response of several transcription factors to immobilization stress was enhanced in the cold adapted animals. RNA will be prepared with RNAqueous-Micro Isolation kit from Ambion (alternatively we can ship the tissues). We will pool samples from 4 rats per treatment to control for variability.

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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Neuronal ire-1 coordinates an organism-wide cold stress response by regulating fat metabolism - Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and ire-1(ok799) Transcriptomes During Cold Stress.

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