Figure 5

URX cell fate is restored by inhibiting apoptosis. (A) Quantification of flp-8::GFP expression in wild type, lin-32(tm1446), ced-3(n717), ced-3(n2452), lin-32(tm1446); ced-3(n717), lin-32(tm1446); ced-3(n2452) and ahr-1(ia3); ced-3(n717); egl-13(ku194) mutant animals. The lin-32(tm1446); ced-3 double mutants partially restore flp-8::GFP expression in the URX neurons. In contrast, in a URX specification factor mutant background the expression of flp-8::GFP cannot be restored by loss of ced-3. N > 85. Note that compound loss of ahr-1(ia3) and egl-13(ku194) causes ~95% loss of flp-8::GFP expression²¹. (B) Quantification of gcy-35::mCherry expression in wild type, lin-32(tm1446), ced-3(n717), ced-3(n2452), lin-32(tm1446); ced-3(n717) and lin-32(tm1446); ced-3(n2452) mutant animals. N > 80. (C) Quantification of gcy-36::GFP expression in wild type, lin-32(tm1446), ced-3(n717), ced-3(n2452), lin-32(tm1446); ced-3(n717) and lin-32(tm1446); ced-3(n2452) mutant animals. N > 90. Statistical significance between wild-type and mutant strains was evaluated using one-way ANOVA analysis. ****P < 0.0001; ***P < 0.0005; **P < 0.005; n.s. not significantly different from control.