Overexpression of ceh-39 rescues XX-specific lethality caused by disruption of other XSE genes

GenotypeaHermaphrodite viability (%)bnc
sex-1(y263); yIs58[ceh-39(+)]/yIs58[ceh-39(+)]d981399
sex-1(y263, RNAi)171304
sex-1(y263, RNAi); yIs58/yIs5871597
fox-1(y303) sex-1(y263)41176
fox-1(y303) sex-1(y263); yIs58/yIs5876784
sex-2(y324) sex-1(y263)e4238
sex-2(y324) sex-1(y263); yIs58/yIs58691286
ceh-39(RNAi) sex-1(y263); yIs58/yIs58f5440
ceh-39(RNAi) fox-1(y303) sex-1(y263); yIs58/yIs58f0480
  • a RNAi was applied as explained in Table 1, footnote a.

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

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

  • d yIs58[ceh-39(+)] is an integrated transgene consisting of multiple copies of a 5.5-kbp genomic fragment spanning the ceh-39 locus.

  • e Data are from C. Y. Loh and B. J. Meyer (personal communication). See footnote d in Table 3.

  • f The rescue of XSE mutants is specific to increased ceh-39 dose because RNAi of ceh-39 not only abolished the suppression caused by yIs58, but also reduced the activity of ceh-39 completely, causing synergistic lethality in combination with XSE mutations.