ASI Regulates Satiety Quiescence in C. elegans

Title
ASI Regulates Satiety Quiescence in C. elegans
Authors
김정호
Issue Date
2013
Publisher
JOURNAL OF NEUROSCIENCE
Series/Report no.
JOURNAL OF NEUROSCIENCE ; Vol33 no.23 Startpage 9716 Endpage 9724
Abstract
In C. elegans, satiety quiescence mimics behavioral aspects of satiety and post-prandial sleep in mammals. On the basis of calcium-imaging, genetics and behavioral studies, here we report that a pair of amphid neurons ASI is activated by nutrition and regulates worms’ behavioral states specifically promoting satiety quiescence; ASI inhibits the switch from quiescence to dwelling (a browsing state) and accelerates the switch from dwelling to quiescence. The canonical TGFβ pathway, whose ligand is released from ASI, regulates satiety quiescence. The mutants of a ligand, a receptor and SMADs in the TGFβ pathway all eat more and show less quiescence than wild type. The TGFβ receptor in downstream neurons RIM and RIC is sufficient for worms to exhibit satiety quiescence, suggesting neuronal connection from ASI to RIM and RIC is essential for feeding regulation through the TGFβ pathway. ASI also regulates satiety quiescence partly through cGMP signaling; restoring cGMP signaling in ASI rescues the satiety quiescence defect of cGMP signaling mutants. From these results, we propose that TGFβ and cGMP pathways in ASI connect nutritional status to promotion of satiety quiescence, a sleep-like behavioral state.
URI
http://dspace.inha.ac.kr/handle/10505/33218
ISSN
0270-6474
Appears in Collections:
College of Natural Science(자연과학대학) > Biological Sciences (생명과학) > Local Access Journal Papers, Reports(생명과학 논문, 보고서)

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