Novel suppressors of vulval rupture in <i>let-7</i> null mutants.

<p>(A) Null <i>let-7(mn112)</i> worms were maintained with an extrachromosomal rescuing transgene (let-7(+)) co-expressing a pharyngeal GFP marker (myo-2::GFP). Progeny that lack the transgene rupture from the vulva and die. (B) The <i>let-7(mn112); Ex[let-7(+);myo-2::GFP]</i> strain was grown on bacteria expressing dsRNA corresponding to candidate targets and the empty vector control. The percent rupture of non-rescued (non-GFP) animals was determined for each RNAi clone. (C) The vector control RNAi fails to suppress vulval rupturing, while knockdown of a known target (<i>daf-12</i>) or a novel candidate (<i>sox-2</i>) allows <i>let-7(mn112)</i> animals to survive to adulthood. (D) The rate of vulval rupture was plotted for each RNAi clone tested. Green points indicate clones that reduced the rupture rate to below 75% in 2/2 experiments (n>50 worms/experiment). Purple points indicate RNAi clones depicted in (C). Red points indicate clones that failed to reproducibly meet the 75% cut-off. The vector negative controls are shown in black.