Changes in lipid metabolism driven by steroid signalling modulate proteostasis in C. elegans

ABSTRACT: Alzheimer's, Parkinson's and Huntington's disease can be caused by mutations that enhance protein aggregation, but we still do not know enough about the molecular players of these pathways to develop treatments for these devastating diseases. Here, we screen for mutations that might enhance aggregation in C. elegans, to investigate the mechanisms that protect against dysregulated homeostasis. We report that the stomatin homologue UNC-1 activates neurohormonal signalling from the sulfotransferase SSU-1 in ASJ sensory/endocrine neurons. A putative hormone, produced in ASJ, targets the nuclear receptor NHR-1, which acts cell-autonomously in the muscles to modulate polyglutamine repeat (polyQ) aggregation. A second nuclear receptor, DAF-12, functions oppositely to NHR-1 to maintain protein hom

SUBMITTER: Dr. Rafael, Pascual Vazquez-Manrique 

PROVIDER: S-SCDT-10_15252-EMBR_202255556 | biostudies-other |

REPOSITORIES: biostudies-other