skn-1 is required for interneuron sensory integration and foraging behavior in Caenorhabditis elegans.

Autor: Wilson MA; Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, United States of America., Iser WB; Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, United States of America., Son TG; Department of Experimental Radiation, Research Center, Dongnam Institute of Radiological and Medical Science, Jwadong-ri, Jangan-eup, Gijang-gun, Busan, Republic of Korea., Logie A; Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, United States of America., Cabral-Costa JV; Department of Pharmacology, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil., Mattson MP; Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, United States of America.; Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America., Camandola S; Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, United States of America.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2017 May 01; Vol. 12 (5), pp. e0176798. Date of Electronic Publication: 2017 May 01 (Print Publication: 2017).
DOI: 10.1371/journal.pone.0176798
Abstrakt: Nrf2/skn-1, a transcription factor known to mediate adaptive responses of cells to stress, also regulates energy metabolism in response to changes in nutrient availability. The ability to locate food sources depends upon chemosensation. Here we show that Nrf2/skn-1 is expressed in olfactory interneurons, and is required for proper integration of multiple food-related sensory cues in Caenorhabditis elegans. Compared to wild type worms, skn-1 mutants fail to perceive that food density is limiting, and display altered chemo- and thermotactic responses. These behavioral deficits are associated with aberrant AIY interneuron morphology and migration in skn-1 mutants. Both skn-1-dependent AIY autonomous and non-autonomous mechanisms regulate the neural circuitry underlying multisensory integration of environmental cues related to energy acquisition.
Databáze: MEDLINE