<i>C. elegans</i> somatostatin/allatostatin C signaling regulates sleep, metabolism, survival, and memory via a sleep-active neuron

coupled and acts cell nonautonomously to activate the sleep-active RIS neuron while acting autonomously in RIS to inhibit calcium activation and the release of the sleep-inducing FLP-11 neuropeptides. During larval arrest, strong NPR-16 expression in RIS causes NLP-99/NPR-16 signaling to inhibit sleep, reducing lipid storage and survival. In well-fed adults, NPR-16 expression is stronger outside of RIS, and NLP-99/NPR-16 signaling is required for RIS activation and sleep while also inhibiting longevity via RIS. Both NLP-99/NPR-16 and RIS/FLP-11 are required for memory consolidation. These results show that NLP-99/NPR-16 regulates physiological processes via control of RIS. A similar somatostatin-mediated regulation of sleep neurons may underlie physiological regulation in other species.

Authors

Institutions

Publication Details

Journal
Science Advances
Published
2026-04-15
DOI
https://doi.org/10.1126/sciadv.adv8387
Primary Topic
Genetics, Aging, and Longevity in Model Organisms
Type
article
Field-Weighted Citation Impact
0.00

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

C. elegans somatostatin/allatostatin C signaling regulates sleep, metabolism, survival, and memory via a sleep-active neuron

Gill Pollmeier, Majdulin Nabil Istiban, Ellen Geens, Attila Steták et al.
Science Advances
Genetics, Aging, and Longevity in Model Organisms
article

C. elegans somatostatin/allatostatin C signaling regulates sleep, metabolism, survival, and memory via a sleep-active neuron

Gill Pollmeier, Majdulin Nabil Istiban, Ellen Geens, Attila Steták, Henrik Bringmann, Isabel Beets, Inka Busack, Lorenzo Rossi, Reshma Dominic Savio, Byoungjun Park, Lama Mohsen, Sajal Mandal, Laura Uhlig
article en

Abstract

coupled and acts cell nonautonomously to activate the sleep-active RIS neuron while acting autonomously in RIS to inhibit calcium activation and the release of the sleep-inducing FLP-11 neuropeptides. During larval arrest, strong NPR-16 expression in RIS causes NLP-99/NPR-16 signaling to inhibit sleep, reducing lipid storage and survival. In well-fed adults, NPR-16 expression is stronger outside of RIS, and NLP-99/NPR-16 signaling is required for RIS activation and sleep while also inhibiting longevity via RIS. Both NLP-99/NPR-16 and RIS/FLP-11 are required for memory consolidation. These results show that NLP-99/NPR-16 regulates physiological processes via control of RIS. A similar somatostatin-mediated regulation of sleep neurons may underlie physiological regulation in other species.

Science AdvancesVol. 12(16)
University of Basel (CH), University Hospital Carl Gustav Carus (DE), Technische Universität Dresden (DE), KU Leuven (BE)
Deutsche Forschungsgemeinschaft, Fonds Wetenschappelijk Onderzoek, KU Leuven, Vlaamse regering, National Institutes of Health, European Research Council
Openalex Percentile: Top 28%
Genetics, Aging, and Longevity in Model Organisms
DOIOpen Access PDFOpenAlex
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.