Troponin I controls ovulatory contraction of non-striated actomyosin networks in the C. elegans somatic gonad

• Type of Material: Article
• Authors: Takashi Obinata, Teikyo-Heisei University; Kanako Ono, Emory University; Shoichiro Ono, Emory University
• Language: English
• Date: 2010-05-01
• Publisher: Company of Biologists
• Publication Version: Final Published Version
• Copyright Statement: © 2010
• Final Published Version (URL): http://jcs.biologists.org/content/123/9/1557
• Title of Journal or Parent Work: Journal of Cell Science
• ISSN: 0021-9533
• Volume: 123
• Issue: 9
• Start Page: 1557
• End Page: 1566
• Grant/Funding Information: Ministry of Education, Science and Culture, Japan (Grant number 20570075) to T.O.; National Institute of Health (R01 AR48615) and University Research Committee of Emory University to S.O.
• Keywords: Myosin; Troponin; Actin; Ovulation; Contraction; Myoepithelial cells
• Research Categories: Biology, Cell; Health Sciences, Pathology

Abstract

The myoepithelial sheath of the Caenorhabditis elegans somatic gonad has non-striated actomyosin networks that provide contractile forces during ovulation, a process in which a mature oocyte is expelled from the ovary. Troponin T and troponin C are known regulators of contraction of the myoepithelial sheath. These are two of the three components of the troponin complex that is generally considered as a striated-muscle-specific regulator of actomyosin contraction. Here, we report identification of troponin I as the third component of the troponin complex that regulates ovulatory contraction of the myoepithelial sheath. C. elegans has four genes encoding troponin-I isoforms. We found that tni-1 and unc-27 (also known as tni-2) encode two major troponin-I isoforms in the myoepithelial sheath. Combination of RNA interference and mutation of tni-1 and unc-27 resulted in loss of the troponin-I protein in the gonad and caused sterility due to defective contraction of the myoepithelial sheath. Troponin-I-depleted gonads were hypercontracted, which is consistent with the function of troponin I as an inhibitor of actomyosin contraction. Troponin I was associated with non-striated actin networks in a tropomyosin-dependent manner. Our results demonstrate that troponin I regulates contraction of non-striated actomyosin networks and is an essential cytoskeletal component of the C. elegans reproductive system.