GSE193923
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.
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. Overall design: Two-condition experiment (control and cold shock), Wild type (N2) C. elegans vs.ire-1(ok799) C. elegans. For control samples, worms were grown at 15 degrees from eggs until day 1 and harvested. For cold shock, worms were grown at 15 degrees from eggs until day 1 and then shifted to 2 degrees for 24 additional hours, and harvested thereafter. Data from 6 biological replicates were used for the N2 wild type strain.  Data from 3 biological replicates were used for the ire-1(ok799) strain.