TABLE 5.
sex-1 functions as an XSE and has an XSE-independent function
| Genotypea | Hermaphrodite viability (%)b | nc |
|---|---|---|
| sex-1(y263) | 70 | 884 |
| xol-1(y9) sex-1(y263) | 87 | 690 |
| sex-1(y263, RNAi) | 17 | 1304 |
| xol-1(y9) sex-1(y263, RNAi) | 58 | 891 |
| sex-1(y424) | 20 | 2308 |
| xol-1(y9) sex-1(y424) | 56 | 1701 |
| sdc-2(RNAi)d | 84 | 1512 |
| sex-1(y263) sdc-2(RNAi)d | 0 | 1072 |
| xol-1(y9) sex-1(y263) sdc-2(RNAi)d | 6 | 2018 |
| xol-1(y9) sdc-2(RNAi)d | 98 | 1211 |
| sdc-2(RNAi)d | 86 | 1244 |
| sex-1(y424) sdc-2(RNAi)d | 0 | 912 |
| xol-1(y9) sex-1(y424) sdc-2(RNAi)d | 0 | 1256 |
| xol-1(y9) sdc-2(RNAi)d | 97 | 1283 |
| dpy-28(RNAi) | 91 | 1439 |
| dpy-28(RNAi); sex-1(y263) | 6 | 2273 |
| dpy-28(RNAi); xol-1(y9) sex-1(y263) | 4 | 1506 |
| dpy-28(RNAi); xol-1(y9) | 89 | 1315 |
| mom-2(RNAi)e | 24 | 1064 |
| mom-2(RNAi); xol-1(y9)e | 58 | 999 |
| unc-22(RNAi)e | 100% viable, 64% Unc | 550 |
| unc-22(RNAi); xol-1(y9)e | 100% viable, 32% Unc | 983 |
Animals were fed bacteria producing dsRNA generated from plasmids encoding the gene listed.
Hermaphrodite viability was calculated by the formula: (no. of adult hermaphrodites)/(total no. of embryos, n) × 100.
n is the total number of embryos from at least six independent sets of progeny counts.
All RNAi treatments and progeny counts performed simultaneously.
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.