About this item:

407 Views | 69 Downloads

Author Notes:

Author for correspondence (sono@emory.edu)

We thank Myeongwoo Lee (Baylor University, Waco, TX) for kindly providing us with the GFP–pat-10 transgenic worms.

Monoclonal antibody 5-6 was developed by Henry Epstein (University of Texas Medical Branch, Galveston), and was obtained from the Developmental Studies Hybridoma Bank, developed under auspices of the NICHD and maintained by the University of Iowa, Department of Biological Sciences, Iowa City, IA. C. elegans strains were provided by Caenorhabditis Genetics Center, which is supported by the National Institute of Health National Center for Research Resources.


Research Funding:

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.


  • Troponin
  • Contraction
  • Ovulation
  • Myoepithelial cells
  • Actin
  • Myosin

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

Journal Title:

Journal of Cell Science


Volume 123, Number 9


, Pages 1557-1566

Type of Work:

Article | Final Publisher PDF


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.

Copyright information:

© 2010

Export to EndNote