Heterochronic protein which controls the choice of stage specific cell fates. Involved in the temporal progression of vulval fate patterning, possibly by inhibiting lin-12. Acts as a transcription factor involved in the stage-specific repression of insulin/insulin-like growth factor gene ins-33. Plays a role in governing the developmental timining of male tail tip morphogenesis (PubMed:26811380, PubMed:30956008). Plays a role in controlling the timing of seam cell development during the larval stages (PubMed:21471153). Plays a role in promoting survival at high temperatures in larvae (PubMed:28250105). Involved in maintenance of the architecture of the ventral nerve cord, perhaps acting via modulating expression of the immunoglobulin domain gene zig-4. May specify L2 and later cell fates, creating a temporal switch. May be involved in specifying L1 cell fates. May associate with mitotic chromosomes. High levels in hypodermal, intestinal, body wall muscle, nerve ring, and ventral nerve cord cells of embryos and L1 animals. Present at high levels in embryos and L1 animals but is undetectable at later stages. Cleaved by caspase ced-3 in vitro. Asynchrony between gonadal and vulval development. Retarded uterine uv1 cell differentiation (PubMed:19161245). 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 in a ced-3 and ain-1 double mutant background reduces the percentage of animals with developmental defects including impaired egg-laying and production of ectopic seam cells (PubMed:25432023). RNAi-mediated knockdown reduced the number of dauer animals in a dcap-1 mutant background (PubMed:28250105).