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. 2016 Apr 1;27(7):1131–1142. doi: 10.1091/mbc.E15-09-0648

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© 2016 Ono and Ono. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 5: — The striated muscle myosin isoform (UNC-54) is partially redundant with the nonmuscle myosin isoform. ppw-1 or unc-54 ppw-1 worms were treated with control RNAi (A, B), mlc-4(RNAi) (C, D), let-502(RNAi) (E, F), or mel-11(RNAi) (G, H). (A–H) Whole worms were stained for F-actin (left) and DNA (middle). Right, merged images (F-actin in red and DNA in blue). Ovulation defects were characterized by the Emo phenotype as indicated by arrows. Positions of the spermatheca are indicated by the letter s. (I) Percentages of worms with ovulation defects as characterized by the Emo phenotype were scored for 100 worms each after 3 d of RNAi treatment. Data are average ± SD (n = 3). Results of a statistical test by one-way ANOVA for comparisons between ppw-1 and unc-54 ppw-1: n. s., not significant (p > 0.05); ***p < 0.001. The unc-54 mutation enhanced the ovulation defect of let-502(RNAi) but partially suppressed that of mel-11(RNAi).