Description |
hlh-2 encodes a Class I basic helix-loop-helix (bHLH) transcription factor that is the C. elegans ortholog of the mammalian E and Drosophila Daughterless transcriptional activators; HLH-2 activity is required for cell fate specifications occuring during embryonic and larval development that affect such processes as gonadogenesis, male tail formation, and programmed cell death; HLH-2 has been shown to dimerize with at least two C. elegans Acheate-scute homologs, LIN-32, a neural-specific protein with which it functions in male tail development and HLH-3, with which it is coexpressed in the nuclei of embryonic neuronal prescursors and with which it regulates the transcription of the EGL-1 cell death activator in the NSM sister cells; in gonadogenesis, HLH-2 is required for bestowing proAC competence on the cells that undergo the AC/VU (anchor cell/ventral uterine precursor) cell fate decision, for specification, differentiation, and function of the distal tip cell (DTC) and AC, including transcriptional regulation of the LAG-2 Delta-like ligand in the latter, and for formation of the uterine seam cell (utse); genetic analysis also suggests that HLH-2 functions with HLH-14, an additional Acaete-scute homolog, to specify the PVQ/HSN/PHB neuroblast cell lineage; HLH-2 is expressed in all nuclei of early embryos until the ~200-cell stage, when expression becomes increasingly restricted to neuronal cells and their immediate precursors; later expression is detected in, but not limited to, pharyngeal cells, anterior neurons, vulval and uterine muscles, the DTCs, the presumptive and mature AC, the Q neuroblast, and enteric muscles; comparative analysis of transcriptional and translational reporters indicates that hlh-2 is expressed in both the anchor cell and the ventral uterine (VU) precursor, but that expression in the latter is subject to post-transcriptional down-regulation; HLH-2 accumulation in the presumptive AC is the first detectable difference between the AC and VU precursors during the lateral specification event that distinguishes these two cell fates. |