Aisa Nakashima et al. (2008) European Worm Meeting "Two new germ cell immortality mutants"

Jan Laroque, Theresa M Zucchero, Julie Hall, Aisa Nakashima, Shawn Ahmed, Lauren Garwood

[European Worm Meeting, 2008]

Germ cells represent canonical stem cells that possess the remarkable. quality of being able to proliferate from one generation to the next,. indefinitely, free of replicative damage. mortal germline mutants initially. display normal levels of fertility, but become progressively sterile when. grown for multiple generations. Of 16 original mortal germline mutants (1),. most were temperature-sensitive and only became sterile when grown at 25oC.. Of the ts mutants, two were resistant to RNAi feeding constructs targeting. embryonic lethal genes at all temperatures: 1c and 10i. The 10i mutation. mapped to the right arm of chromosome IV, between unc-22 and dpy-4, and. fails to complement rsd-2 for its RNAi resistance phenotype. rsd-2 has been. reported to be is deficient for spreading of dsRNA-mediated RNAi from. somatic cells to germ cells (2), suggesting that this function may be. relevant to maintaining germ cells over multiple generations during growth. at high temperatures. The mechanism by which this occurs is being studied.. (1) Ahmed S, Hodgkin J (2000). MRT-2 checkpoint protein is required for. germline immortality and telomere replication in C. elegans. Nature.. (2) Tijsterman M, May RC, Simmer F, Okihara KL, Plasterk RH (2004). Genes. required for systemic RNA interference in Caenorhabditis elegans. Current. Biology.

Shi, Cheng et al. (2019) International Worm Meeting "Insulin-like peptides and the mTOR-TFEB pathway protect C. elegans hermaphrodites from Mating-induced Death."

Shi, Cheng, Murphy, Coleen

[International Worm Meeting, 2019]

C. elegans lifespan is shortened by mating, but must be delayed long enough for successful reproduction. Susceptibility to brief mating-induced death increases with age; surprisingly, this is not due to declining health, but to loss of protection upon self-sperm depletion. Self-sperm maintains expression of a DAF-2 insulin-like antagonist, INS-37, which promotes the nuclear localization of HLH-30/TFEB, a 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, increasing the chances that mothers will survive through reproduction. The hijacking of the IIS pathway by males is combated by the mother's expression of an insulin antagonist that keeps her healthy through the activity of pro-longevity factors, as long as she has her own sperm to utilize. ** If possible, I would prefer that this abstract please be considered with the abstract submitted by Lauren N. Booth, Travis J. Maures, Robin W. Yeo, and Anne Brunet ("Self-sperm induce resistance to the detrimental effects of sexual encounters with males in hermaphroditic nematodes").