High impact information on egl-1

• Gain-of-function (gf) mutations in egl-1 cause the inappropriate programmed cell death of the HSNs in hermaphrodites [1].
• The TRA-1A sex determination protein of C. elegans regulates sexually dimorphic cell deaths by repressing the egl-1 cell death activator gene [1].
• 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 [1].
• The egl-1 gene negatively regulates the ced-9 gene, which protects against cell death and is a member of the bcl-2 family [2].
• Whereas egl-1 animals appear to be defective specifically in HSN development, her-1(n695) animals exhibit multiple morphological pleiotropies, displaying partial transformation of the sexual phenotype of many cells and tissues [3].

Biological context of egl-1

• Direct regulation of egl-1 and of programmed cell death by the Hox protein MAB-5 and by CEH-20, a C. elegans homolog of Pbx1 [4].

Anatomical context of egl-1

• However, this machinery is activated by a distinct pathway, as loss of egl-1 function, which inhibits somatic cell death, does not affect germ cell apoptosis [5].

Associations of egl-1 with chemical compounds

• The gene egl-1 encodes a BH3-containing cell death activator that is required for programmed cell death in C. elegans [1].

References