him-8(e1489) suppresses the male tail defect and defective hindgut expression of a lin-48∷GFP reporter but exacerbates the vulval development and egg-laying defects caused by egl-38(gu22). The histogram illustrates the percentage of animals that express lin-48::GFP in at least one of the four hindgut cells with normal male tail morphology, normal vulval morphology, or normal egg-laying activity (Egl⁺). Phenotypes were assayed as reported (Chamberlin et al. 1997; Johnson et al. 2001; Zhang et al. 2005; Rajakumar and Chamberlin 2007).

Mutation of him-8 suppresses non-null mutations in the DNA-binding domains of POP-1, SPTF-3, and LIN-39. The histogram illustrates the percentage of normal phenotypes. The percentage of normal pop-1(q624) animals reported here agrees closely with previously published data (Siegfried and Kimble 2002). We also scored these phenotypes in pop-1(q624); syIs50[cdh-3∷GFP] and pop-1(q624);e1489; syIs50[cdh-3∷GFP] animals and obtained similar results (data not shown). cdh-3∷GFP is strongly expressed in the anchor cell, allowing easier scoring of the double-anchor cell defect. Note that 100% of wild-type animals are Egl⁺ and have one anchor cell and two gonad arms.

him-8(e1489) increases the intensity of lin-48∷GFP expression in the hindgut of an egl-38(gu22) mutant. (A) Fluorescent image of the hindgut region of an saIs14[lin-48∷GFP] hermaphrodite overlaid on the corresponding DIC image. (B) lin-48∷GFP expression is visible in four hindgut cells that flank the rectum. (C) Expression is consistently detected in all four cells at similar intensities in the transgenic parent strain. (D) The intensity of lin-48∷GFP expression in him-8(e1489); saIs14[lin-48∷GFP] animals is not detectably different from that of the parent strain. (E) Thirty-one percent of egl-38(gu22); unc-119(e2498); saIs14[lin-48∷GFP] animals lack all hindgut expression of lin-48∷GFP (Figure 3), and the intensity of lin-48∷GFP expression is weaker than that of the parental strain in all animals that have expression. (F) In addition to an increase in the percentage of the population that expresses the reporter faithfully (Figure 3), all suppressed egl-38(gu22) him-8(e1489); saIs14[lin-48∷GFP] animals have an increase in the intensity of lin-48∷GFP expression relative to the parental strain. Image exposure conditions were identical for A and C–F.

Mutation of the zim genes suppresses the Cog and Egl defects of egl-13(ku207). The histogram illustrates the Cog⁺ and Egl⁺ percentage of egl-13(ku207) and suppressor; egl-13(ku207) double mutants. The original zim-3(tm2303) chromosome was associated with linked mutations causing lethality (Phillips and Dernburg 2006). Thus, we used an unc-24(e138) zim-3(tm2303) recombinant chromosome, which causes less lethality (Phillips and Dernburg 2006), to assay suppression by zim-3 and tested unc-24(e138) as a control. Cog and Egl phenotypes were scored as reported (Hanna-Rose and Han 1999). The him-8(e1489) data were published previously (Nelms and Hanna-Rose 2006) and shown here for comparison. Note that wild-type animals have 100% normal gonad morphology and egg-laying ability. For Figures 1–3, basic principles of proportional analysis were applied as previously described to obtain 95% confidence intervals shown as error bars (Nelms and Hanna-Rose 2006). Actual percentage is cited within each bar, and sample sizes (n) are indicated at the right in Figures 1–3. Asterisks indicate values for double mutants in Figures 1–3 that are significantly different from the relevant single mutants (P < 0.005, Fisher's exact test).