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Unilateral dampening of Bmp activity by Nodal generates cardiac left-right asymmetry

Official URL:https://doi.org/10.1016/j.devcel.2013.01.026
PubMed:View item in PubMed
Creators Name:Veerkamp, J. and Rudolph, F. and Cseresnyes, Z. and Priller, F. and Otten, C. and Renz, M. and Schaefer, L. and Abdelilah-Seyfried, S.
Journal Title:Developmental Cell
Journal Abbreviation:Dev Cell
Volume:24
Number:6
Page Range:660-667
Date:25 March 2013
Keywords:Body Patterning, Bone Morphogenetic Proteins, Cell Movement, Developmental Gene Expression Regulation, Glucuronosyltransferase, Heart, Left-Right Determination Factors, Nodal Protein, Nonmuscle Myosin Type IIA, Nonmuscle Myosin Type IIB, Signal Transduction, Zebrafish Proteins, Animals, Zebrafish
Abstract:Signaling by Nodal and Bmp is essential for cardiac laterality. How activities of these pathways translate into left-right asymmetric organ morphogenesis is largely unknown. We show that, in zebrafish, Nodal locally reduces Bmp activity on the left side of the cardiac field. This effect is mediated by the extracellular matrix enzyme Hyaluronan synthase 2, expression of which is induced by Nodal. Unilateral reduction of Bmp signaling results in lower expression of nonmuscle myosin II and higher cell motility on the left, driving asymmetric displacement of the entire cardiac field. In silico modeling shows that left-right differences in cell motility are sufficient to induce a robust, directional migration of cardiac tissue. Thus, the mechanism underlying the formation of cardiac left-right asymmetry involves Nodal modulating an antimotogenic Bmp activity.
ISSN:1534-5807
Publisher:Cell Press (U.S.A.)
Item Type:Article

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