Guanyl-specific endoribonuclease which cleaves the phosphodiester bond in single-stranded RNA between the 3'-guanylic residue and the 5'-OH residue of adjacent nucleotide, resulting in the formation of a corresponding 2',3'-cyclic phosphate intermediate (PubMed:26787882). Together with the P-granule component pgl-3, is involved in the formation of P-granules (PubMed:21402787, PubMed:24746798). Together with pgl-3, probably recruits other granule components such as pos-1, mex-3 and glh-1 to P-granules (PubMed:21402787). In addition, may act redundantly with pgl-3 to protect germ cells from excessive germline apoptosis during normal oogenesis and development of the two gonadal arms (PubMed:26598553). This may in part be through regulating the localization of sir-2.1 which is involved in germ cell apoptosis (PubMed:26598553). May protect somatic cells from excessive apoptosis during normal development (PubMed:27650246). Essential role in male and female postembryonic germline development; maternally provided protein maintains a population of proliferating germ cells and zygotic expression is required for correct oogenesis (PubMed:9741628, PubMed:15238518, PubMed:24746798). [RNA] containing guanosine + H2O = an [RNA fragment]-3'-guanosine-3'-phosphate + a 5'-hydroxy-ribonucleotide-3'-[RNA fragment]. Does not require metal ions for catalytic activity. Not inhibited by RNase inhibitor RNasin. Homodimer (PubMed:15238518, PubMed:26787882). Interacts with pgl-2 and pgl-3; this association is not required for P-granule localization of either pgl-2 or pgl-3 (PubMed:15238518). Interacts with ife-1 (PubMed:11641215, PubMed:15238518). Interacts with prmt-1; the interaction is direct (PubMed:24140420). Interacts with nmad-1 (PubMed:31283754). Interacts with P granule components meg-1, meg-3 and meg-4 (PubMed:25535836). Localizes to P granules in germline precursor cells (PubMed:9741628, PubMed:19167332, PubMed:24140420, PubMed:27650246, PubMed:28806108). Localizes to P granules in germ cells at all stages of development except in spermatogenesis (PubMed:15238518). Co-localizes with pgl-3 in P-granules, but localization in P-granules is not dependent on an association with pgl-3 (PubMed:15238518, PubMed:21402787). At P-granules in the adult germline, co-localizes with deps-1 in the pachytene region and with prg-1 (PubMed:32843637). Expressed in the germline (PubMed:9741628, PubMed:15238518). Expressed in most somatic cells (PubMed:27650246). Expressed throughout development from embryos to adults (PubMed:9741628, PubMed:15238518, PubMed:27650246). Not expressed in somatic cells of embryos (PubMed:28806108). First expressed in 1-cell embryos, and expression persists until the 4-cell stage (PubMed:15238518). Expression diminishes in somatic blastomeres, but remains in E and P3 blastomeres at the 8-cell stage, in P3 blastomeres at the 15-cell stage, and in P4 blastomeres at the 24-cell stage (PubMed:15238518). Expressed in the primordial germ cells Z2 and Z3 during the two-fold stage of embryogenesis (PubMed:15238518, PubMed:27650246). Levels are low in young larvae but increase at the end of larval development (PubMed:9741628). Expressed in germ blastomeres (PubMed:19377305). The dimerization domain also acts as a hinge; changes in its structure probably impact oligomerization and RNA-binding. The RNA-binding RGG-box is required for the recruitment of some P-granule components such as pos-1 and probably mRNA, but is dispensable for granule formation. Methylated at arginine residues in the RNA-binding RGG-box by prmt-1. Methylation promotes P-granule degradation by autophagy. Temperature-sensitive and are only fertile at 20 degrees Celsius (PubMed:26787882). 25% of progeny arresting as late embryos and 9% as larvae at 26 degrees Celsius (PubMed:15238518). Surviving progeny are sterile at 26 degrees Celsius, most likely due to germline proliferation defects (PubMed:9741628, PubMed:15238518, PubMed:26787882). The temperature-sensitive period extends from mid-larvae to young adults (PubMed:9741628). Germline defects include increased apoptosis in the gonad, fewer germ nuclei, no sperm and no oocytes in the gonad arms (PubMed:15238518, PubMed:26598553). Double knockout with pgl-3 results in 37% of progeny arresting as late embryos and 9% as larvae at 26 degrees Celsius (PubMed:15238518). Double knockout with pgl-3 enhances the temperature-sensitive sterility phenotype and germline defects of the pgl-1 single knockout (PubMed:15238518, PubMed:26598553). The gonads of the double knockout with pgl-3 degenerate as the adults age (PubMed:15238518). Triple knockout with pgl-2 and pgl-3 results in 58% of progeny arresting as late embryos and 5% as larvae at 26 degrees Celsius (PubMed:15238518). Double knockout with him-3 decreases the number of self-cross progeny in the him-3 single mutant (PubMed:15238518). Triple knockout with pgl-3 and him-3 further reduces the number of self-cross progeny as compared to the pgl-1 and him-3 double mutant and him-3 single mutant (PubMed:15238518). Double knockout with ced-1 results in an increased number of cell corpses in the gonad as compared to the ced-1 single mutant (PubMed:26598553). Conversely, double knockout with ced-1 results in reduced somatic cell apoptosis (PubMed:27650246). Triple knockout with ced-1 and hpl-2 partially recovers the reduced somatic cell apoptotic cell defect in the ced-1 and hpl-2 double knockout (PubMed:27650246). Triple knockout with ced-1 and hpl-2 and knockdown with either ced-3 or ced-4 reduces the somatic cell apoptosis defect in the ced-1, hpl-2 and pgl-1 triple knockout (PubMed:27650246). Double RNAi-mediated knockdown with pgl-1 results in a reduced number of pos-1, mex-1 and glh-1 positive granules in embryos (PubMed:21402787). Quadruple RNAi-mediated knockdown with glh-1, glh-4 and pgl-3 results in offspring that display 27-89% sterility, abnormal oocytes and do not have embryos in the uterus (PubMed:24746798). These sterile offspring still produce sperm (PubMed:24746798). Furthermore, these offspring may have compromised P-granule integrity as there is diffuse cytoplasmic localization of the P-granule component deps-1, which may cause germ cells to initiate somatic reprogramming (PubMed:24746798). RNAi-mediated knockdown in a double ced-1 and hpl-2 mutant background rescues the reduced somatic cell apoptotic cell defect in the ced-1 and hpl-2 double knockout (PubMed:27650246).