gld-1, a tumor suppressor gene required for oocyte development in Caenorhabditis elegans.

TLDR

The study infers gld‑1’s role from a haplo‑insufficient phenotype and gain‑of‑function mutations that alter germ cell sexual identity. The authors identified 31 gld‑1 mutations, showing that null hermaphrodites lack oogenesis and develop germline tumors while males are unaffected; tumors arise from germ cells that exit pachytene and re‑enter mitosis, and partial loss‑of‑function mutants arrest in pachytene, establishing gld‑1 as a tumor suppressor essential for oocyte development and, additionally, promoting hermaphrodite spermatogenesis.

Abstract

Abstract We have characterized 31 mutations in the gld-1 (defective in germline development) gene of Caenorhabditis elegans. In gld-1 (null) hermaphrodites, oogenesis is abolished and a germline tumor forms where oocyte development would normally occur. By contrast, gld-1 (null) males are unaffected. The hermaphrodite germline tumor appears to derive from germ cells that enter the meiotic pathway normally but then exit pachytene and return to the mitotic cycle. Certain gld-1 partial loss-of-function mutations also abolish oogenesis, but germ cells arrest in pachytene rather than returning to mitosis. Our results indicate that gld-1 is a tumor suppressor gene required for oocyte development. The tumorous phenotype suggests that gld-1(+) may function to negatively regulate proliferation during meiotic prophase and/or act to direct progression through meiotic prophase. We also show that gld-1(+) has an additional nonessential role in germline sex determination: promotion of hermaphrodite spermatogenesis. This function of gld-1 is inferred from a haplo-insufficient phenotype and from the properties of gain-of-function gld-1 mutations that cause alterations in the sexual identity of germ cells.