Figure S13.
rpoa-2(
op259) suppresses excessive apoptosis in
rad-51(lf) and
abl-1(lf) mutants. A) Current model of apoptosis induction in C. elegans. Two modes have classically been distinguished for the apoptotic death of germ cells, mainly by their dependence on
cep-1 and
egl-1. During somatic development, transcriptional regulation of EGL-1 is key for the lineage-specific induction of most cell deaths. EGL-1 physically disrupts the inhibitory binding of CED-9 to CED-4, which in turn serves as platform for CED-3 activation [9]. For DNA damage-induced germ cell death, EGL-1 and CED-13 are transcriptionally up-regulated by CEP-1/p53. By contrast, physiological germ cell death is largely CEP-1- and EGL-1-independent.
abl-1(lf) and
rad-51(lf) were shown to increase CEP-1 dependent cell death [10], [11]. B) Apoptotic response to IR irradiation (60 Gy) in the
abl-1(
ok171) kinase mutant background. Error bars, CI 95% of the mean number of germ cell corpses per gonad (n = 15). C) Baseline apoptosis (0 Gy, straight lines) and response to IR irradiation (60 Gy, dashed lines) in the
rad-51(
lg8701) DNA repair-mutant background.
rad-51(
lg8701) homozygous animals were derived from the balanced strains
rad-51(
lg8701)/nT1 and
rpoa-2(
op259);
rad-51(
lg8701)/nT1 and irradiated as young adults. Error bars, CI 95% of the mean number of germ cell corpses per gonad (n = 15).