DAF-18/PTEN is an important tumour suppressor, and loss of PTEN activity is associated with various types of cancers. In C. elegans hermaphrodites that lack sperm, such as
fog-1 mutants, DAF-18 is required for oocytes to arrest and accumulate in the proximal gonad. As such,
fog-1;
daf-18 double mutants lay unfertilised oocytes, and fail to downregulate germline stem cell (GSC) proliferation. However, the tissue(s) in which DAF-18 acts to permit oocyte arrest and accumulation in the absence of sperm, and to eventually suppress GSC proliferation, is still unknown. Here, we transgenically rescued
daf-18, specifically in the gut, neurons, hypodermis, muscles, proximal somatic gonad, and germline, of
fog-1;
daf-18 null mutants. Interestingly, we found that
daf-18 expression in the muscles, or in the proximal somatic gonad, was sufficient to allow unfertilized oocytes to arrest and accumulate in the proximal gonad of
fog-1;
daf-18 double mutants. DAF-18 is also required to suppress the proliferation of germ and somatic gonadal cells during dauer formation, wherein DAF-18 acts in the somatic gonadal cells. Using our germline-specific DAF-18 transgene, we further show that maternally-provided DAF-18 is sufficient to rescue the dauer phenotype of
daf-18(-) mutants, but not the arrest of unfertilized oocytes in spermless adults. Overall, our results demonstrate that DAF-18 can act from at least two separate tissues to non-autonomously mediate the arrest of oocytes in the absence of sperm, and allow for their accumulation in the proximal gonad. These results may provide new insights into the how PTEN prevents tumour formation.