RT Journal Article
SR Electronic
T1 ASI Regulates Satiety Quiescence in <em>C. elegans</em>
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 9716
OP 9724
DO 10.1523/JNEUROSCI.4493-12.2013
VO 33
IS 23
A1 Gallagher, Thomas
A1 Kim, Jeongho
A1 Oldenbroek, Marieke
A1 Kerr, Rex
A1 You, Young-Jai
YR 2013
UL http://www.jneurosci.org/content/33/23/9716.abstract
AB In Caenorhabditis elegans, satiety quiescence mimics behavioral aspects of satiety and postprandial 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.