Component of the egl-1, ced-9, ced-4 and ced-3 apoptotic signaling cascade required for the initiation of programmed cell death in cells fated to die during embryonic and postembryonic development. During oogenesis, required for germline apoptosis downstream of ced-9 and upstream of ced-3 but independently of egl-1. May regulate germline apoptosis in response to DNA damage, probably downstream of let-60/ras and mpk-1 pathway. Regulates CEP neuron apoptosis in response to high Al(3+) levels. During male tail morphogenesis, promotes apoptosis of the tail-spike cell upstream of ced-3 but independently of egl-1 and ced-9. May play a role in sex-specific cell apoptosis, probably by promoting ced-3-mediated cleavage of sex-determining protein fem-1. During larval development, required for the elimination of transient presynaptic components downstream of egl-1 and ced-9 and upstream of ced-3 apoptotic pathway. Downstream of calreticulin crt-1 and upstream of ced-3 and independently of egl-1 and ced-9, plays a role in the initial steps of axonal regrowth following axotomy. Together with ain-1, a component of the miRNA-induced-silencing complex (miRISC), and probably upstream of ced-3, regulates temporal cell fate patterning during larval development. May play a role in resistance to S.typhimurium-mediated infection.; Plays a major role in programmed cell death. egl-1 binds to and directly inhibits the activity of ced-9, releasing the cell death activator ced-4 from a ced-9/ced-4 containing protein complex and allowing ced-4 to induce caspase ced-3 autoproteolytic cleavage and activation. Also forms a holoenzyme with processed ced-3 enhancing ced-3 activity.; Prevents programmed cell death.
