Transcriptional repressor which interacts with the promoter region of target genes (PubMed:25032706). Has a specific role in developmental timing where it regulates temporal expression of a number of miRNAs and mRNAs (PubMed:16300753, PubMed:25032706, PubMed:25319259, PubMed:15691769, PubMed:29880558). Controls temporal cell fate transition during embryonic and early larval development by restricting the expression of specific miRNAs, including let-7, miR-48, lin-4, miR-35 and miR-58 (PubMed:24699545, PubMed:25032706, PubMed:25319259, PubMed:15691769, PubMed:29880558). Restricts the accumulation of lin-29 in the hypodermis to the larval L4 stage, thus controlling terminal differentiation of seam cells (PubMed:10550049, PubMed:21471153). Has a role in the miRNA-mediated specification of asymmetric gene expression patterns in gustatory neurons (PubMed:25032706). May also regulate genes involved in other biological processes including transport, small molecule metabolism, and growth (PubMed:25032706). Inhibits dauer formation, by antagonizing daf-12 (PubMed:20843862). Specifically required for maintaining the timing of larval development and molting cycle rhythms. Expression is generally more enriched in the nuclei than the cytoplasm (PubMed:10550049). Cytoplasmic expression is enhanced in lateral seam cells during the molt periods of larval development (PubMed:16300753). Additional isoforms seem to exist. Expressed from late embryonic stage onwards (PubMed:10550049, PubMed:16300753). Shows oscillating expression levels during larval stages, with peak levels in intermolt periods and minimal levels during ecdysis (PubMed:16300753, PubMed:20843862, PubMed:22137474, PubMed:29880558). Expressed in hypodermis, vulva, intestine, muscle, neurons and somatic gonad throughout larval development, in an oscillating pattern (PubMed:16300753, PubMed:22137474). Expressed in sex myoblasts during larval stages L1, L2 and L3, in an oscillating pattern (PubMed:16300753). Expressed in gonad distal tip cells (DTC) during the L2 and L3 stages, in an oscillating pattern (PubMed:16300753). Expressed in the pharyngeal myoepithelium, the major body hypodermal syncytium and lateral seam cells from the mid L1 stage. Expression in the hypodermis rises and falls at the start and end of every molt, respectively. Mutants exhibit a delay in development characterized by a strong molting defect, resulting in a prolonged L1 stage followed by an arrest in development in the L2 stage in most animals (PubMed:25319259). There is increased expression of the heterochronic miRNAs, lin-4 and miR-48, in late L1 (PubMed:25319259). In addition, there is increased expression of the heterochronic miRNA let-7 at the L3 and L4 larval stages (PubMed:29880558). Seam cell shape and connectivity is severely abnormal during the molt stages (PubMed:22137474). Animals display a precocious alae phenotype, with the early formation of either full or partial alae in the adult cuticle (PubMed:25319259, PubMed:29880558). The precocious alae phenotype is suppressed in the double lin-42 and let-7 mutant and lin-42 and miR-48 mutant (PubMed:25319259). The quadruple lin-42, miR-48, miR-241 and let-7 mutant has a retarded phenotype at L4, with many animals having few full and partial alae or none (PubMed:25319259). The number of animals displaying a squat body statue, referred to as a dumpy phenotype, is increased, the incomplete alae formation defect is rescued and increased let-7 levels are reduced in a kin-20 RNAi-mediated knockdown mutant background (PubMed:29880558). RNAi-mediated knockdown leads to a severe hypodermal phenotype, premature execution of developmental events in vulval precursor cells, DTC and sex myoblasts (PubMed:16300753). Furthermore, seam cell terminal differentiation is only partially initiated at the L4 larval stage (PubMed:15691769). RNAi-mediated knockdown increases the survival rate and partially restores alae formation of let-7 n2853 mutants at 20 degrees Celsius (PubMed:15691769). Produced by alternative promoter usage. Produced by alternative splicing.