Probable ATP-binding RNA helicase (PubMed:8415696). May act redundantly with the P-granule component glh-4 to regulate the formation of the granular structure of P-granules in embryos (PubMed:21402787, PubMed:24746798). Plays a role in positively regulating the localization of pgl-1 to P-granules (PubMed:18234720). May play a role in transgenerational epigenetic inheritance (PubMed:28533440). May protect somatic cells from excessive apoptosis during normal development (PubMed:27650246). ATP + H2O = ADP + H(+) + phosphate Interacts with csn-5; this may prevent glh-1 degradation induced by kgb-1 (PubMed:12435362, PubMed:17699606). Interacts with zyx-1 (PubMed:12435362). Interacts (via the N-terminal region containing the four CCHC zinc fingers) with pan-1 (PubMed:22342905). Interacts with kgb-1; this may promote glh-1 degradation by the proteasome (PubMed:17699606). Perinuclear localization in germ cells but disperses into particles in cellularized oocytes. Component of P granules. First expressed during the L3-L4 stages of larval development, coinciding with germline proliferation. Phosphorylated by kgb-1 (in vitro); this may be responsible for its degradation by the proteasome. Mortal germline (Mrt) phenotype in which there is a progressive decline in fertility with each generation at 25 degrees Celsius (PubMed:28533440). RNAi-mediated knockdown in a glh-4 mutant background results in smaller P-granules and irregular cytoplasmic localization of the P-granule component pgl-3 in embryos (PubMed:21402787). Quadruple RNAi-mediated knockdown with glh-4, pgl-1 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). Belongs to the DEAD box helicase family. DDX4/VASA subfamily.