Murat Artan1, Dae-Eun Jeong2, Dongyeop Lee2, Young-Il Kim1,2,6, Heehwa G. Son2, Zahabiya Husain3, Jinmahn Kim4, Ozlem Altintas5, Kyuhyung Kim4, Joy Alcedo3 and Seung-Jae V. Lee1,2,5 *
1Information Technology Convergence Engineering, Pohang University of Science and Technology, Pohang, Gyeongbuk 37673, South Korea;
2Department of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk 37673, South Korea;
3Department of Biological Sciences, Wayne State University, Detroit, Michigan 48202, USA;
4Department of Cognitive and Brain Sciences, DGIST (Daegu Gyeongbuk Institute of Science and Technology), Daegu 42988, South Korea;
5School of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology, Pohang, Gyeongbuk 37673, South Korea
6 Present address: Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, South Korea.
Environmental fluctuations influence organismal aging by affecting various regulatory systems. One such system involves sensory neurons, which affect life span in many species. However, how sensory neurons coordinate organismal aging in response to changes in environmental signals remains elusive. Here, we found that a subset of sensory neurons shortens Caenorhabditis elegans’ life span by differentially regulating the expression of a specific insulin-like peptide (ILP), INS-6. Notably, treatment with food-derived cues or optogenetic activation of sensory neurons significantly increases ins-6 expression and decreases life span. INS-6 in turn relays the longevity signals to nonneuronal tissues by decreasing the activity of the transcription factor DAF-16/FOXO. Together, our study delineates a mechanism through which environmental sensory cues regulate aging rates by modulating the activities of specific sensory neurons and ILPs.