The hermaphrodite-specific neurons (HSNs) of the nematode Caenorhabditis elegans are generated embryonically in both hermaphrodites and males but undergo programmed cell death in males. The gene
egl-1 encodes a BH3-containing cell death activator that is required for programmed cell death in C. elegans. Gain-of-function (gf) mutations in
egl-1 cause the inappropriate programmed cell death of the HSNs in hermaphrodites. These mutations lie 5.6 kb downstream of the
egl-1 transcription unit and disrupt the binding of the TRA-1A zinc finger protein, the terminal global regulator of somatic sexual fate. This disruption results in the activation of the
egl-1 gene in the HSNs not only in males but also in hermaphrodites. Our findings suggest that in hermaphrodites TRA-1A represses
egl-1 transcription in the HSNs to prevent these neurons from undergoing programmed cell death.AD - Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge 02319, USA.FAU - Conradt, BAU - Conradt BFAU - Horvitz, H RAU - Horvitz HRLA - engID - GM24663/GM/NIGMSPT - Journal ArticleCY - UNITED STATESTA - CellJID - 0413066RN - 0 (DNA, Helminth)RN - 0 (EGL-1 protein)RN - 0 (Helminth Proteins)RN - 0 (Luminescent Proteins)RN - 0 (Oligodeoxyribonucleotides)RN - 0 (Repressor Proteins)RN - 0 (TRA-1A protein)RN - 0 (Transcription Factors)RN - 147336-22-9 (green fluorescent protein)SB - IM