RT Journal Article
SR Electronic
T1 Neuronal SKN-1B Modulates Nutritional Signalling Pathways and Mitochondrial Networks to Control Satiety
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.07.21.213504
DO 10.1101/2020.07.21.213504
A1 Nikolaos Tataridas-Pallas
A1 Maximillian Thompson
A1 Alexander Howard
A1 Ian Brown
A1 Marina Ezcurra
A1 Ziyun Wu
A1 Timo Keurten
A1 Isabel Goncalves Silva
A1 T. Keith Blackwell
A1 Jennifer Tullet
YR 2020
UL http://biorxiv.org/content/early/2020/07/27/2020.07.21.213504.abstract
AB The feeling of hunger or satiety results from integration of the sensory nervous system with other physiological and metabolic cues. This regulates food intake, maintains homeostasis and prevents disease. In C. elegans, chemosensory neurons sense food and relay information to the rest of the animal via hormones to control food-related behaviour and physiology. Here we identify a new component of this system, SKN-1B which acts as a central food-responsive node, ultimately controlling satiety and metabolic homeostasis. SKN-1B, an ortholog of mammalian NF-E2 related transcription factors (Nrfs), has previously been implicated with metabolism and respiration, because can mediate the increased lifespan incurred by dietary restriction. We show that actually SKN-1B is not essential for dietary restriction longevity and instead, controls a variety of food-related behaviours. It acts in two hypothalamus-like ASI neurons to sense food, communicate nutritional status to the organism, and control satiety and exploratory behaviours. This is achieved by SKN-1B modulating endocrine signalling pathways (IIS and TGF-β), and by promoting a robust mitochondrial network. Our data suggest a food-sensing and satiety role for mammalian Nrf proteins.Competing Interest StatementThe authors have declared no competing interest.