First published online November 3, 2003
Development 130, e2406 (2003)
Copyright © 2003 The Company of Biologists Limited
Be still my beating heart
Changes in functional demand can alter the morphology of the adult heart;
for example, pressure overload can induce ventricular hypertrophy. Now, two
groups of researchers provide evidence that blood flow also affects cardiac
morphology during embryogenesis. Berdougo et al. have investigated the effect
of a mutation in the gene atrial myosin heavy chain on heart
development in zebrafish (see p.
6121). Although this gene is expressed only in the atrium, mutations
in it result in not only atrial contractile defects but also ventricular
morphological defects. Similarly, Huang et al. report that inactivation of the
gene for atrial myosin light chain 2 in mice causes severely diminished atrial
contraction and secondary abnormalities in cardiac morphogenesis (see
p. 6111). Both research teams
conclude that alterations in blood flow caused by the mis-functioning of one
embryonic heart chamber epigenetically influence the morphogenesis of the
other chamber, and they discuss how these findings may provide clues to the
causes of human congenital heart defects.
Related articles in Development:
- Embryonic atrial function is essential for mouse embryogenesis, cardiac morphogenesis and angiogenesis
- Chengqun Huang, Farah Sheikh, Melinda Hollander, Chengleng Cai, David Becker, Po-Hsien Chu, Sylvia Evans, and Ju Chen
Development 2003 130: 6111-6119.
[Abstract]
[Full Text]
- Mutation of weak atrium/atrial myosin heavy chain disrupts atrial function and influences ventricular morphogenesis in zebrafish
- Eli Berdougo, Hope Coleman, Diana H. Lee, Didier Y. R. Stainier, and Deborah Yelon
Development 2003 130: 6121-6129.
[Abstract]
[Full Text]
