ArticleeLife2019
Insulin-like peptides and the mTOR-TFEB pathway protect
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
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- C. elegans ageing is accelerated by a self-destructive reproductive programme.Nature communications · 2023Article
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- Intestine-to-neuronal signaling alters risk-taking behaviors in food-deprived Caenorhabditis elegans.PLoS genetics · 2022Article
- Transgenerational inheritance of sexual attractiveness via small RNAs enhances evolvability in C. elegans.Developmental cell · 2022Article
- Structural recognition of the mRNA 3' UTR by PUF-8 restricts the lifespan of C. elegans.Nucleic acids research · 2021Article
- Reproductive Aging inFrontiers in cell and developmental biology · 2021Review
- FoxO directly regulates the expression of TOR/S6K and vitellogenin to modulate the fecundity of the brown planthopper.Science China. Life sciences · 2021Article
- Oleic Acid ProtectsFrontiers in cell and developmental biology · 2021Article
- Mating in the absence of fertilization promotes a growth-reproduction versus lifespan trade-off in female mice.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Being open to the unexpected.Molecular biology of the cell · 2019Article
- A new defense in the battle of the sexes.eLife · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Lifespan is shortened by mating, but these deleterious effects must be delayed long enough for successful reproduction. Susceptibility to brief mating-induced death is caused by the loss of protection upon self-sperm depletion. Self-sperm maintains the expression of a DAF-2 insulin-like antagonist, INS-37, which promotes the nuclear localization of intestinal HLH-30/TFEB, a key pro-longevity regulator. Mating induces the agonist INS-8, promoting HLH-30 nuclear exit and subsequent death. In opposition to the protective role of HLH-30 and DAF-16/FOXO, TOR/LET-363 and the IIS-regulated Zn-finger transcription factor PQM-1 promote seminal-fluid-induced killing. Self-sperm maintenance of nuclear HLH-30/TFEB allows hermaphrodites to resist mating-induced death until self-sperm are exhausted, increasing the chances that mothers will survive through reproduction. Mothers combat males' hijacking of their IIS pathway by expressing an insulin antagonist that keeps her healthy through the activity of pro-longevity factors, as long as she has her own sperm to utilize.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.