ASI regulates satiety quiescence in C. elegans.
J Neurosci
; 33(23): 9716-24, 2013 Jun 05.
Article
em En
| MEDLINE
| ID: mdl-23739968
ABSTRACT
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 TGFß pathway, whose ligand is released from ASI, regulates satiety quiescence. The mutants of a ligand, a receptor and SMADs in the TGFß pathway all eat more and show less quiescence than wild-type. The TGFß 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 TGFß 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 TGFß and cGMP pathways in ASI connect nutritional status to promotion of satiety quiescence, a sleep-like behavioral state.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Proteínas Quinases
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Células Receptoras Sensoriais
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Saciação
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Caenorhabditis elegans
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Proteínas de Caenorhabditis elegans
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Ingestão de Alimentos
Limite:
Animals
Idioma:
En
Revista:
J Neurosci
Ano de publicação:
2013
Tipo de documento:
Article
País de afiliação:
Estados Unidos