Nakashima, Aisa et al. (2009) International Worm Meeting "RNAi Spreading Mutants rsd-2 and rsd-6 are Deficient for Germ Cell Immortality."

Ahmed, Shawn, Garwood, Lauren, Nakashima, Aisa, Alvares, Stacy, Hall, Julie, LaRoque, Jan, Zucchero, Theresa

[International Worm Meeting, 2009]

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 (mrt) mutants initially display normal levels of fertility, but become progressively sterile when grown for multiple generations. Of 16 mrt mutants identified in a pilot EMS screen (Ahmed and Hodgkin, 2000), most were temperature-sensitive and only became sterile when grown at 25 deg C. Of the ts mutants, two were resistant to RNAi feeding constructs targeting embryonic lethal genes: 1c and 10i. Genetic mapping experiments, complementation tests for RNAi resistance, and DNA sequencing revealed that 1c and 10i contain mutations in rsd-6 and rsd-2, respectively. Independently isolated alleles of rsd-6 and rsd-2 confer progressive sterility when propagated at 25 deg C, and complementation tests confirmed that these genes are required for germ cell immortality. rsd-6 and rsd-2 have been reported to be deficient for spreading of dsRNA-mediated RNAi from somatic cells to germ cells (Tijsterman et al., 2004). However, our results indicate that RSD-6 may be required in germ cells to promote germ cell immortality, whereas it functions in somatic but not germ cells to promote RNAi spreading. In addition, other RNAi-spreading defective mutants do not exhibit progressive sterility. These results indicate that RSD-6 and RSD-2 are likely to promote germ cell immortality via a mechanism that is distinct from their role in RNAi spreading.

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").