Severe hypothermia is often lethal. Yet, hibernating animals survive cold while radically reducing brain functions, become “diabetic” but fully recover from it, slow down aging, etc. Understanding how animals can do that is a fascinating question with potential biomedical implications, ranging from emergency medicine to space travel. Studying both nematodes and mammalian cells, we uncover a conserved mechanism improving cold survival, potentially opening an avenue to improved treatments of hypothermia.
Regnase-1 is a widely studied RNase. It degrades mRNAs important for many biological processes, including immune homeostasis, development, and cancer. There are two competing models of Regnase-1-mediated mRNA decay. One model postulates that Regnase-1 is recruited to mRNA targets by another RNA-binding protein, Roquin. The other model proposes that the two proteins function separately. In this paper, we show a conserved functional connection between Regnase-1 and Roquin counterparts in C. elegans but also highlight species-specific differences. This provides a rare perspective on the evolution of an important post-transcriptional regulatory mechanism.