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. 2007 Nov;177(3):1621–1637. doi: 10.1534/genetics.106.061812

TABLE 5.

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

Genotypea Hermaphrodite viability (%)b nc
sex-1(y263) 70 884
sex-1(y263); yIs58[ceh-39(+)]/yIs58[ceh-39(+)]d 98 1399
sex-1(y263, RNAi) 17 1304
sex-1(y263, RNAi); yIs58/yIs58 71 597
fox-1(y303) sex-1(y263) 4 1176
fox-1(y303) sex-1(y263); yIs58/yIs58 76 784
sex-2(y324) sex-1(y263)e 4 238
sex-2(y324) sex-1(y263); yIs58/yIs58 69 1286
ceh-39(RNAi) sex-1(y263); yIs58/yIs58f 5 440
ceh-39(RNAi) fox-1(y303) sex-1(y263); yIs58/yIs58f 0 480
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.