Probable transcription factor, required for migration of the hermaphrodite-specific motor neurons (HSNs) from the tail to the gonad primordium during HSN cell differentiation (PubMed:8224840, PubMed:10049362). Required for phasmid neuron development (PubMed:8224840). Required to specify the pi-cell fate of ventral uterine precursor cell (VU) cells (PubMed:17573066). Probable transcription factor, involved in lin-12 (Notch)-dependent anchor cell (AC) and ventral uterine (VU) precursor cell fate specification and in AC invasion (PubMed:17215301, PubMed:17573066, PubMed:32203506). Prevents AC proliferation after AC cell specification by repressing lin-12 expression (PubMed:32203506). May form a positive feedback loop, together with the transcription factor fos-1, that maintains mutual high levels of expression and so activates AC invasion (PubMed:32203506). Dispensable for anchor cell (AC) invasion and for preventing AC proliferation. Expressed in the hermaphrodite-specific motor neuron (HSN) / phasmid sensory neuron B (PHB) precursor, and the phasmid sensory neuron A (PHA) in the tail at ~400 minutes embryogenesis (at protein level) (PubMed:10049362). Continues to be expressed in PHA and PHB neurons of L1 larvae (PubMed:10049362). Expressed in the HSN before and during HSN migration from the tail to the gonad primordium of the embryo and down-regulated after migration (at protein level) (PubMed:10049362). Expressed in the pre-anchor cell (AC)/pre-ventral uterine (VU) cells at early L2 and maintained in their 37 descendants at early L4 (PubMed:17215301, PubMed:32203506). Expressed in the ventral uterine (VU) cells of mid L2 larvae (Pn.p stage) and then in the anchor cell (AC) beginning in mid L3 larvae (PubMed:17573066, PubMed:32203506). Expression increases during AC invasion (PubMed:17573066). Expressed, earlier than isoform a, in the anchor cell (AC) at the Pn.p stage in mid L2 larvae (PubMed:17573066). Expression decreases during AC invasion (PubMed:17573066). The positive regulatory (PR) domain is required for egl-43 protein stability but is dispensable for anchor cell (AC) invasion and preventing AC proliferation. The C2H2-type zinc-finger domains 1, 2 and 3 are dispensable for anchor cell (AC) invasion and preventing AC proliferation. The C2H2-type zinc-finger domains 4 and 5 may be required for anchor cell (AC) invasion and preventing AC proliferation. RNAi-mediated knockdown causes defects in anchor cell (AC) and ventral uterine (VU) precursor cell specification and AC invasion in the larval L3 and L4 stages (PubMed:17215301, PubMed:17573066). RNAi-mediated knockdown on a lin-12 mutant background reverses the AC-deficient phenotype (PubMed:17215301). RNAi-mediated knockdown reduces expression of zmp-1, cdh-3 and him-4 in the AC (PubMed:17215301, PubMed:17573066). RNAi-mediated knockdown reduces expression of fos-1a in the anchor cell (AC) approximately three-fold (PubMed:32203506). RNAi-mediated knockdown causes defects in vulval morphogenesis (PubMed:17573066). RNAi-mediated knockdown causes defects in anchor cell (AC) invasion, including increased CDK activity and re-entry of the AC into the cell cycle, resulting in the presence of two or more AC. No defects in anchor cell (AC) invasion or arrest in G1 seen upon RNAi-mediated knockdown.