Heterochronic protein which acts downstream of let-7 in temporal patterning (PubMed:10882102, PubMed:30910805). Plays a role in the developmental timing of postembryonic hypodermal seam cell division and fusion events and adult alae production (PubMed:28933985). Represses lin-29 during late larval stages, which prevents terminal differentiation of hypodermal seam cells and promotes their division (PubMed:10882102). Involved in post-transcriptional gene regulation, uses two independent pathways (PubMed:28157501). Has direct and specific RNA-binding activity and, depending on the location (5'UTR or 3'UTR) of the target site, triggers either mRNA decay or repression of translation (PubMed:28111013, PubMed:30910805). Degrades the mRNA of transcription factor dmd-3 to govern the timing and extent of male tail tip morphogenesis (PubMed:16806150, PubMed:18550714, PubMed:28111013, PubMed:30910805, PubMed:26811380, PubMed:30956008). Plays a role in the sexual maturation of the nervous system (PubMed:31264582). Expressed in body wall muscles, pharyngeal muscles and most neurons at all stages from late embryogenesis until adulthood. Expressed in hypodermal seam cells until the L4 stage. Negatively regulated by the microRNA (miRNA) let-7 which causes degradation of the mRNA encoding this protein. This requires a let-7 complementary site (LCS) in the 3'-UTR of the mRNA encoding this protein. The NHL domain, containing the 6 NHL repeats, is necessary and sufficient to target RNA but not to repress mRNA. The minimal region needed to execute repression consists of the coiled coil domain and the Filamin repeat. The RING-type domain is dispensable for mRNA repression. RNAi-mediated knockdown results in the precocious onset of tail tip retraction resulting in over-retracted and shortened adult male tails (also known as the Ore phenotype) (PubMed:26811380, PubMed:30956008). RNAi-mediated knockdown results in increased expression of dmd-3. Belongs to the TRIM/RBCC family.