Transciptional regulator which is involved in the sex determination and X chromosome dosage compensation pathways (PubMed:21471153, PubMed:23666922, PubMed:16139225, PubMed:17720939, PubMed:33372658). Directly binds to five 5'-A(G/C)(G/T)(T/G)C(A/G)-3' sites in the promoter of sex-determining factor xol-1 to negatively regulate its expression and promote hermaphrodite development (PubMed:23666922). Together with fox-1 is involved in making the distinction between one and two X-chromosomes (PubMed:21471153, PubMed:23666922, PubMed:33372658). Plays a role in the fox-1-mediated repression of the functionally active isoform (isoform b) of the sex-determining factor xol-1 gene to promote hermaphrodite development (PubMed:33372658). Plays a role in the association of the dosage compensation complex proteins dpy-27 and sdc-3 with the hermaphrodite X chromosomes (PubMed:16139225, PubMed:17720939). Most abundant in embryos. RNAi-mediated knockdown results in 43% lethality of hermaphrodites (PubMed:33372658). RNAi-mediated knockdown together with fox-1 results in hermaphrodite embryonic lethality (PubMed:21471153, PubMed:33372658). This hermaphrodite-specific lethality is suppressed in a sea-2 bp283 mutant or sea-1 gk799 mutant background (PubMed:21471153). RNAi-mediated knockdown results in hermaphrodites lethality due to failure of the dosage compensation complex to assemble on X chromosomes in a fox-1 y303 mutant background (PubMed:17720939). RNAi-mediated knockdown in a background containing one copy of the fox-1 gene results in the viability of 3% of hermaphrodites (PubMed:33372658). RNAi-mediated knockdown in a strain where all of the GCACG and GCUAG motifs in intron 6 of the xol-1 gene have been mutated to AUACA and AUAUA, respectively results in the viability of 1% of hermaphrodites (PubMed:33372658). RNAi-mediated knockdown in a strain where all of the GCACG and GCUAG motifs in intron 6 of one copy of the xol-1 gene have been mutated to AUACA and AUAUA, respectively results in the viability of 7% of hermaphrodites (PubMed:33372658). RNAi-mediated knockdown in a strain where all of the GCACG motifs in intron 6 of the xol-1 gene have been mutated to AUACA results in the viability of 24% of hermaphrodites (PubMed:33372658). RNAi-mediated knockdown in a strain where all of the GCACG motifs in intron 6 of one copy of the xol-1 gene have been mutated to AUACA results in the viability of 18% of hermaphrodites (PubMed:33372658). RNAi-mediated knockdown in a strain where all of the GCUAG motifs in intron 6 of the xol-1 gene have been mutated to AUAUA results in the viability of 33% of hermaphrodites (PubMed:33372658). RNAi-mediated knockdown in a strain where all of the GCUAG motifs in intron 6 of one copy of the xol-1 gene have been mutated to AUAUA results in the viability of 13% of hermaphrodites (PubMed:33372658). RNAi-mediated knockdown in a strain where all of the GCACG and GCUAG motifs in intron 6 of the xol-1 gene have been mutated to GCUUG results in the viability of 8% of hermaphrodites (PubMed:33372658). RNAi-mediated knockdown in a strain where all of the GCACG and GCUAG motifs in intron 6 of one copy of the xol-1 gene have been mutated to GCUUG results in the viability of 36% of hermaphrodites (PubMed:33372658). RNAi-mediated knockdown in strains containing five or three fox-1-binding GCACG motifs in intron 6 of the xol-1 gene results in the viability of 49% and 33% of hermaphrodites, respectively (PubMed:33372658). Belongs to the nuclear hormone receptor family. NR1 subfamily.