Insulin signaling in Caenorhabditis elegans regulates both endocrine-like and cell-autonomous outputs
Open accessAbstract
In C. elegans, insulin signaling affects development, lifespan and stress resistance. Several studies have shown that insulin signaling affects lifespan in an endocrine-like manner from different cells, while the major downstream target of insulin, the FOXO transcription factor encoded by daf-16, may act preferentially in intestinal cells to prolong lifespan. This discrepancy raised the possibility that insulin may have both endocrine and cell-intrinsic outputs. Here, we further investigated the types of cells capable of producing endocrine outputs of insulin and also identified a new cell-intrinsic insulin output. We found that insulin signaling within groups of neurons promoted wildtype lifespan, showing that the endocrine outputs of insulin were not restricted to specific cells. In contrast, DAF-16 appeared to have a greater effect on lifespan when expressed in a combination of tissues. These results suggest that insulin signaling may regulate DAF-16 through cell-intrinsic and endocrine pathways. We also found that an insulin-dependent response to fasting in intestinal cells was preferentially regulated by intestinal insulin signaling and was less responsive to insulin signaling from non-intestinal cells. Together, these results show that C. elegans insulin signaling has endocrine as well as tissue-specific outputs which could influence lifespan in a combinatorial fashion.
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Reduced IIS specifically in the nervous system is sufficient to extend lifespan in several model systems.
“Importantly, reduced IIS specifically in the nervous system is sufficient to extend lifespan in several model systems.”
From Neural mechanisms of ageing and cognitive decline (2010) · cites this paper as [66]
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- Authors
- Iser, W. B., Gami, M. S., & Wolkow, C. A.
- Affiliations
- National Institute on Aging (US)
- Corresponding author
- Wolkow, Catherine A.
- Venue
- Developmental Biology
- Publisher
- Elsevier BV
- Published
- 2007-03
- Volume
- 303
- Issue
- 2
- Pages
- 434-447
- ISSN
- 0012-1606 (ISSN-L)
- PMC
- PMC2262836
- OpenAlex
- W2070586322
- Cited by
- 48
- References
- 45
- Citations by year
- 2025: 3 · 2024: 2 · 2023: 5 · 2022: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 4 · 2015: 1 · 2014: 2 · 2013: 2 · 2012: 3
- FWCI
- 0.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Ellison Medical Foundation
- National Institutes of Health
- National Institute on Aging (Z01AG000320)
- Institute of Genetics
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurobiology and Insect Physiology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- insulin signaling, Caenorhabditis elegans, DAF-16, FOXO transcription factors, lifespan regulation, fasting response, tissue-specific gene expression
- MeSH terms
- Aging, Animals, Fasting, Insulin, Longevity, Models, Biological, Mutation, Neurons, Transcription Factors, Signal Transduction, Caenorhabditis elegans, Genes, Helminth, Phosphatidylinositol 3-Kinases, Caenorhabditis elegans Proteins, Animals, Genetically Modified, Forkhead Transcription Factors
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