RT Journal Article
SR Electronic
T1 Olfactory chemosensation extends lifespan through TGF-β signaling and UPR activation
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2022.10.12.511902
DO 10.1101/2022.10.12.511902
A1 De-Souza, Evandro A.
A1 Thompson, Maximillian A.
A1 Taylor, Rebecca C.
YR 2022
UL http://biorxiv.org/content/early/2022/10/12/2022.10.12.511902.abstract
AB Animals rely on chemosensory cues to survive in pathogen-rich environments. In C. elegans, pathogenic bacteria are known to trigger aversive behaviors through neuronal perception, and to activate molecular defenses throughout the animal. This suggests that neurons may be able to coordinate the activation of organism-wide defensive responses upon pathogen perception. We find that exposure to volatile pathogen-associated compounds induces cell non-autonomous activation of the endoplasmic reticulum unfolded protein response (UPRER) in peripheral tissues following xbp-1 splicing in neurons. This odorant-induced UPRER activation is dependent upon transforming growth factor beta (TGF-β) signaling and leads to extended lifespan and enhanced clearance of toxic proteins. Our data suggest that the cell non-autonomous UPRER rewires organismal proteostasis in response to pathogen detection, pre-empting the arrival of proteotoxic stress. Thus, chemosensation of particular odors may be a novel way to manipulate stress responses and longevity.Competing Interest StatementThe authors have declared no competing interest.