sex-1 functions as an XSE and has an XSE-independent function

GenotypeaHermaphrodite viability (%)bnc
xol-1(y9) sex-1(y263)87690
sex-1(y263, RNAi)171304
xol-1(y9) sex-1(y263, RNAi)58891
xol-1(y9) sex-1(y424)561701
sex-1(y263) sdc-2(RNAi)d01072
xol-1(y9) sex-1(y263) sdc-2(RNAi)d62018
xol-1(y9) sdc-2(RNAi)d981211
sex-1(y424) sdc-2(RNAi)d0912
xol-1(y9) sex-1(y424) sdc-2(RNAi)d01256
xol-1(y9) sdc-2(RNAi)d971283
dpy-28(RNAi); sex-1(y263)62273
dpy-28(RNAi); xol-1(y9) sex-1(y263)41506
dpy-28(RNAi); xol-1(y9)891315
mom-2(RNAi); xol-1(y9)e58999
unc-22(RNAi)e100% viable, 64% Unc550
unc-22(RNAi); xol-1(y9)e100% viable, 32% Unc983
  • a Animals were fed bacteria producing dsRNA generated from plasmids encoding the gene listed.

  • b Hermaphrodite viability was calculated by the formula: (no. of adult hermaphrodites)/(total no. of embryos, n) × 100.

  • c n is the total number of embryos from at least six independent sets of progeny counts.

  • d All RNAi treatments and progeny counts performed simultaneously.

  • e The xol-1(y9) mutation appears to reduce the effectiveness of RNAi against some genes. mom-2 encodes the WNT signaling molecule; loss of mom-2 function causes embryonic lethality. unc-22 encodes a muscle protein; loss of unc-22 function causes a twitching phenotype. xol-1(y9) reduces the effectiveness of mom-2(RNAi) and unc-22(RNAi). This phenomenon probably accounts for why 84% of sdc-2(RNAi) animals are viable, but 98% of xol-1; sdc-2 (RNAi) animals are viable. The xol-1(y9) mutation probably reduces the effectiveness of sdc-2(RNAi). However, xol-1(y9) does not suppress the lethality of sdc-2 mutants. The ability of xol-1(y9) to interfere with RNAi against some genes does not compromise any of our conclusions. First, xol-1(y9) suppresses the lethality caused by the sex-1(y424) null mutation (see Table 3) to the same degree that it suppresses the lethality caused by sex-1(RNAi) (this table). Second, suppression of XX lethality in sdc-2(RNAi) sex-1(y263) or dpy-28(RNAi); sex-1(y263) animals by xol-1(y9) is very poor, and the ineffectiveness of RNAi in xol-1(y9) could cause only the opposite effect: the extent of suppression would be greater than it would otherwise be.