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Two distinct myosin II populations coordinate ovulatory contraction of the myoepithelial sheath in the Caenorhabditis elegans somatic gonad.

Ono K, Ono S - Mol. Biol. Cell (2016)

Bottom Line: MLC-4, a nonmuscle myosin regulatory light chain, localizes to small punctate structures and does not colocalize with large, needle-like myosin filaments containing MYO-3, a striated-muscle myosin isoform.RNA interference of MLC-4, as well as of its upstream regulators, LET-502 (Rho-associated coiled-coil forming kinase) and MEL-11 (a myosin-binding subunit of myosin phosphatase), impairs ovulation.A striated-muscle myosin (UNC-54) appears to provide partially compensatory contractility.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology and Department of Cell Biology, Emory University, Atlanta, GA 30322.

No MeSH data available.


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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).
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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).

Mentions: Control RNAi did not cause ovulation defects in ppw-1 or unc-54(s95) ppw-1 (Figure 5, A, B, and J), whereas mlc-4(RNAi) caused 100% ovulation defects in either ppw-1 or unc-54(s95); ppw-1 (Figure 5, C, D, and I). However, ovulation defects caused by RNAi of let-502 (ROCK) were greatly enhanced by the unc-54(s95) mutation in both appearance of the endomitotic oocytes (compare Figure 5, E and F) and occurrence of ovulation-defective worms (Figure 5I). This result suggests that the low penetrance of the let-502(RNAi) phenotype was partly due to an alternative actomyosin contractility produced by UNC-54. In contrast, the rate of ovulation defects caused by RNAi of mel-11 (myosin-binding subunit of MRLC phosphatase) was slightly reduced by the unc-54(s95) mutation (Figure 5I), although the appearance of the endomitotic oocytes was not obviously altered (Figure 5, G and H). Therefore reduced contractility by the unc-54(s95) mutation could counterbalance excessive contractility due to lack of MLC-4 dephosphorylation, which partially suppresses the ovulation defects. Together these results suggest that each of the two myosin II populations provides partially compensatory actomyosin contractility of the myoepithelial sheath and that proper regulation of the two myosin systems is essential for successful ovulation in C. elegans.


Two distinct myosin II populations coordinate ovulatory contraction of the myoepithelial sheath in the Caenorhabditis elegans somatic gonad.

Ono K, Ono S - Mol. Biol. Cell (2016)

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).
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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).
Mentions: Control RNAi did not cause ovulation defects in ppw-1 or unc-54(s95) ppw-1 (Figure 5, A, B, and J), whereas mlc-4(RNAi) caused 100% ovulation defects in either ppw-1 or unc-54(s95); ppw-1 (Figure 5, C, D, and I). However, ovulation defects caused by RNAi of let-502 (ROCK) were greatly enhanced by the unc-54(s95) mutation in both appearance of the endomitotic oocytes (compare Figure 5, E and F) and occurrence of ovulation-defective worms (Figure 5I). This result suggests that the low penetrance of the let-502(RNAi) phenotype was partly due to an alternative actomyosin contractility produced by UNC-54. In contrast, the rate of ovulation defects caused by RNAi of mel-11 (myosin-binding subunit of MRLC phosphatase) was slightly reduced by the unc-54(s95) mutation (Figure 5I), although the appearance of the endomitotic oocytes was not obviously altered (Figure 5, G and H). Therefore reduced contractility by the unc-54(s95) mutation could counterbalance excessive contractility due to lack of MLC-4 dephosphorylation, which partially suppresses the ovulation defects. Together these results suggest that each of the two myosin II populations provides partially compensatory actomyosin contractility of the myoepithelial sheath and that proper regulation of the two myosin systems is essential for successful ovulation in C. elegans.

Bottom Line: MLC-4, a nonmuscle myosin regulatory light chain, localizes to small punctate structures and does not colocalize with large, needle-like myosin filaments containing MYO-3, a striated-muscle myosin isoform.RNA interference of MLC-4, as well as of its upstream regulators, LET-502 (Rho-associated coiled-coil forming kinase) and MEL-11 (a myosin-binding subunit of myosin phosphatase), impairs ovulation.A striated-muscle myosin (UNC-54) appears to provide partially compensatory contractility.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology and Department of Cell Biology, Emory University, Atlanta, GA 30322.

No MeSH data available.


Related in: MedlinePlus