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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.


Related in: MedlinePlus

MLC-4, LET-502, and MEL-11 are essential for ovulation. ppw-1 worms were treated with control RNAi (A, E), mlc-4(RNAi) (B, F), let-502(RNAi) (C, G), or mel-11(RNAi) (D, H). (A–D) 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 presence of endomitotic oocytes (Emo) with large DNA accumulations in the ovary, as indicated by arrows. Positions of the spermatheca are indicated by the letter s. Both mlc-4(RNAi) and mel-11(RNAi) caused severe Emo phenotypes, whereas let-502(RNAi) led to somewhat weaker Emo phenotypes. (E–H) Dissected gonads were stained for F-actin (left) and MYO-3 (middle). Right, merged images (F-actin in red and MYO-3 in green). These RNAi treatments did not cause major disorganization of the actin-MYO-3 network. (I) Pearson’s coefficient for F-actin and MYO-3 quantified as a measurement of colocalization and shown as average ± SD (n = 10). Results of a statistical test by one-way ANOVA for comparisons with control RNAi; n. s., not significant (p > 0.05); *0.05 > p > 0.01. Only mel-11(RNAi) increased the F-actin-MYO-3 colocalization significantly, suggesting that contraction was induced.
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Figure 2: MLC-4, LET-502, and MEL-11 are essential for ovulation. ppw-1 worms were treated with control RNAi (A, E), mlc-4(RNAi) (B, F), let-502(RNAi) (C, G), or mel-11(RNAi) (D, H). (A–D) 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 presence of endomitotic oocytes (Emo) with large DNA accumulations in the ovary, as indicated by arrows. Positions of the spermatheca are indicated by the letter s. Both mlc-4(RNAi) and mel-11(RNAi) caused severe Emo phenotypes, whereas let-502(RNAi) led to somewhat weaker Emo phenotypes. (E–H) Dissected gonads were stained for F-actin (left) and MYO-3 (middle). Right, merged images (F-actin in red and MYO-3 in green). These RNAi treatments did not cause major disorganization of the actin-MYO-3 network. (I) Pearson’s coefficient for F-actin and MYO-3 quantified as a measurement of colocalization and shown as average ± SD (n = 10). Results of a statistical test by one-way ANOVA for comparisons with control RNAi; n. s., not significant (p > 0.05); *0.05 > p > 0.01. Only mel-11(RNAi) increased the F-actin-MYO-3 colocalization significantly, suggesting that contraction was induced.

Mentions: RNA interference of mlc-4 in ppw-1 mutant caused accumulation of endomitotic oocytes in the proximal ovary (Emo phenotype) in 100 ± 0.0% (n = 3; 100 worms were scored in each experiment; Figure 2B, arrow), which is typically a result of repeated DNA replication cycles due to defective ovulation (Iwasaki et al., 1996). Control RNAi in ppw-1 did not cause significant abnormalities in the gonad (Emo phenotype, 0.67 ± 0.56%; n = 3; 100 worms scored in each experiment; Figure 2A), indicating that the ppw-1 mutation did not affect the ovulation process. Of interest, the overall architecture of the networks of actin filaments and MYO-3 in the myoepithelial sheath was largely intact after depletion of MLC-4 (compare Figure 2, E and F), suggesting that MLC-4 is involved in contractility but not assembly of the actomyosin network.


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)

MLC-4, LET-502, and MEL-11 are essential for ovulation. ppw-1 worms were treated with control RNAi (A, E), mlc-4(RNAi) (B, F), let-502(RNAi) (C, G), or mel-11(RNAi) (D, H). (A–D) 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 presence of endomitotic oocytes (Emo) with large DNA accumulations in the ovary, as indicated by arrows. Positions of the spermatheca are indicated by the letter s. Both mlc-4(RNAi) and mel-11(RNAi) caused severe Emo phenotypes, whereas let-502(RNAi) led to somewhat weaker Emo phenotypes. (E–H) Dissected gonads were stained for F-actin (left) and MYO-3 (middle). Right, merged images (F-actin in red and MYO-3 in green). These RNAi treatments did not cause major disorganization of the actin-MYO-3 network. (I) Pearson’s coefficient for F-actin and MYO-3 quantified as a measurement of colocalization and shown as average ± SD (n = 10). Results of a statistical test by one-way ANOVA for comparisons with control RNAi; n. s., not significant (p > 0.05); *0.05 > p > 0.01. Only mel-11(RNAi) increased the F-actin-MYO-3 colocalization significantly, suggesting that contraction was induced.
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Related In: Results  -  Collection

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Figure 2: MLC-4, LET-502, and MEL-11 are essential for ovulation. ppw-1 worms were treated with control RNAi (A, E), mlc-4(RNAi) (B, F), let-502(RNAi) (C, G), or mel-11(RNAi) (D, H). (A–D) 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 presence of endomitotic oocytes (Emo) with large DNA accumulations in the ovary, as indicated by arrows. Positions of the spermatheca are indicated by the letter s. Both mlc-4(RNAi) and mel-11(RNAi) caused severe Emo phenotypes, whereas let-502(RNAi) led to somewhat weaker Emo phenotypes. (E–H) Dissected gonads were stained for F-actin (left) and MYO-3 (middle). Right, merged images (F-actin in red and MYO-3 in green). These RNAi treatments did not cause major disorganization of the actin-MYO-3 network. (I) Pearson’s coefficient for F-actin and MYO-3 quantified as a measurement of colocalization and shown as average ± SD (n = 10). Results of a statistical test by one-way ANOVA for comparisons with control RNAi; n. s., not significant (p > 0.05); *0.05 > p > 0.01. Only mel-11(RNAi) increased the F-actin-MYO-3 colocalization significantly, suggesting that contraction was induced.
Mentions: RNA interference of mlc-4 in ppw-1 mutant caused accumulation of endomitotic oocytes in the proximal ovary (Emo phenotype) in 100 ± 0.0% (n = 3; 100 worms were scored in each experiment; Figure 2B, arrow), which is typically a result of repeated DNA replication cycles due to defective ovulation (Iwasaki et al., 1996). Control RNAi in ppw-1 did not cause significant abnormalities in the gonad (Emo phenotype, 0.67 ± 0.56%; n = 3; 100 worms scored in each experiment; Figure 2A), indicating that the ppw-1 mutation did not affect the ovulation process. Of interest, the overall architecture of the networks of actin filaments and MYO-3 in the myoepithelial sheath was largely intact after depletion of MLC-4 (compare Figure 2, E and F), suggesting that MLC-4 is involved in contractility but not assembly of the actomyosin network.

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