The TRA-1A sex determination protein of C. elegans regulates sexually dimorphic cell deaths by repressing the egl-1 cell death activator gene.

Abstract

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.