RNA-binding protein which functions together with alg-1, a component of the miRNA loading complex, to modulate the processing and activity of specific miRNAs such as miR-58 and let-7 to regulate gene expression at the post-transcriptional level during embryonic, hypodermal and neuronal development (PubMed:31584932). Promotes the lsy-6-mediated repression of cog-1 in uterine cells (PubMed:31584932). In embryos, may play a role in the DNA damage response (PubMed:15654100). Interacts with alg-1; the interaction is direct and may be strengthened through RNA-protein association. Localizes to the cytoplasm and nucleus in the germline, oocytes and early embryos (PubMed:31584932). Does not localize to the cytoplasm of somatic cells (PubMed:31584932). Expressed in gut, muscle, neuronal and hypodermal tissues (PubMed:31584932). Highly expressed in the germline and oocytes (PubMed:31584932). Ubiquitously expressed throughout development (PubMed:31584932). Highly expressed in early embryos (PubMed:31584932). Temperature sensitive with 35% embryonic lethality at 20 degrees Celsius and 80% at 25 degrees Celsius (PubMed:31584932). Of the surviving offspring, 30% are sterile at 20 degrees Celsius and 76% are sterile at 25 degrees Celsius (PubMed:31584932). The majority of non-sterile animals have a reduced brood size (PubMed:31584932). In addition, animals have gonadal formation defects and display a bursting vulva phenotype (PubMed:31584932). Reduced number of miRNAs including miR-58 in embryos and L4 larvae (PubMed:31584932). Defective neuronal cell fate switching, whereby fewer ASEL neurons adopt an ASER cell fate in an lsy-6 mutant background (PubMed:31584932). In young adults, increased number of seam cells and enhanced hypodermal development defects in the double miR-48 and miR-241 mutant (PubMed:31584932). The majority of mutants are embryonic lethal in a miR-35-42 mutant background (PubMed:31584932). Enhanced defects in hypodermal development and alae formation in a let-7 mutant background (PubMed:31584932). RNAi-mediated knockdown relieves the lys-6-mediated repression of cog-1 in uterine cells (PubMed:31584932). RNAi-mediated knockdown results in increased sensitivity to the DNA-damage agent methyl methanesulfonate in embryos, but does not disrupt the morphology of the nucleus (PubMed:15654100). RNAi-mediated knockdown enhances the bursting vulva phenotype in a let-7 mutant background (PubMed:31584932).