AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol (January 23, 2003). doi:10.1152/ajpheart.00947.2002
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Submitted on November 4, 2002
Accepted on January 17, 2003

E-Tmod Capping of Actin Filaments at the Slow-Growing End Is Required to Establish Mouse Embryonic Circulation

Xin Chu1, Ju Chen2, Mary C Reedy3, Carlos J Vera1, K.-L. Paul Sung4, and L. Amy Sung1*

1 Department of Bioengineering, University of California San Diego, La Jolla, CA, USA
2 Department of Medicine, University of California San Diego, La Jolla, CA, USA
3 Department of Orthopedics, University of California San Diego, La Jolla, CA, USA
4 Department of Cell Biology, Duke University, Durham, NC, USA; Department of Bioengineering, University of California San Diego, La Jolla, CA, USA

* To whom correspondence should be addressed. E-mail: amysung{at}bioeng.ucsd.edu.

Tropomodulins are a family of proteins that cap the slow-growing end of actin filaments. Erythrocyte tropomodulin (E-Tmod) stabilizes short actin protofilaments in erythrocytes and caps longer sarcomeric actin filaments in striated muscles. We report the knock-in of lacZ under the control of the endogenous E-Tmod promoter and the knockout of E-Tmod in mouse embryonic stem cells. E-Tmod -/- embryos die around E10 and exhibit a non-contractile heart tube with disorganized myofibrils and underdevelopment of the right ventricle, accumulation of mechanically weakened primitive erythroid cells in the yolk sac and failure of primary capillary plexuses to remodel into vitelline vessels required to establish blood circulation between the yolk sac and the embryo proper. We propose a hemodynamic "plexus channel selection" mechanism as the basis for vitelline vascular morphogenesis. The defects in cardiac contractility, vitelline circulation, and hematopoiesis reflect an essential role for E-Tmod capping of the actin filaments in both assembly of cardiac sarcomeres and of the membrane cytoskeleton in erythroid cells that is not compensated for by other proteins.




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