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Am J Physiol Heart Circ Physiol 284: H1827-H1838, 2003. First published January 23, 2003; doi:10.1152/ajpheart.00947.2002
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Vol. 284, Issue 5, H1827-H1838, May 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. Reedy4, Carlos Vera1, K.-L. Paul Sung3, and Lanping Amy Sung1

1 Department of Bioengineering, 2 Department of Medicine, and 3 Department of Orthopedics, University of California-San Diego, La Jolla, California 92093-0412; and 4 Department of Cell Biology, Duke University, Durham, North Carolina 27710

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 knockin of the beta -galactosidase gene (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 embryonic day 10 and exhibit a noncontractile 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, all 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 remodeling. 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 skeleton in erythroid cells that is not compensated for by other proteins.

erythrocyte tropomodulin; cardiomorphogenesis; hematopoiesis; LacZ; yolk sac; vasculogenesis


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