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J. Cardiovasc. Dev. Dis. 2015, 2(1), 2-16;

Cellular Mechanisms of Drosophila Heart Morphogenesis

Development, Aging and Regeneration Program, Sanford-Burnham Medical Research Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA
Author to whom correspondence should be addressed.
Academic Editor: Silke R. Sperling
Received: 6 December 2014 / Revised: 7 February 2015 / Accepted: 11 February 2015 / Published: 16 February 2015
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Many of the major discoveries in the fields of genetics and developmental biology have been made using the fruit fly, Drosophila melanogaster. With regard to heart development, the conserved network of core cardiac transcription factors that underlies cardiogenesis has been studied in great detail in the fly, and the importance of several signaling pathways that regulate heart morphogenesis, such as Slit/Robo, was first shown in the fly model. Recent technological advances have led to a large increase in the genomic data available from patients with congenital heart disease (CHD). This has highlighted a number of candidate genes and gene networks that are potentially involved in CHD. To validate genes and genetic interactions among candidate CHD-causing alleles and to better understand heart formation in general are major tasks. The specific limitations of the various cardiac model systems currently employed (mammalian and fish models) provide a niche for the fly model, despite its evolutionary distance to vertebrates and humans. Here, we review recent advances made using the Drosophila embryo that identify factors relevant for heart formation. These underline how this model organism still is invaluable for a better understanding of CHD. View Full-Text
Keywords: Drosophila; cardiogenesis; morphogenesis; tinman; Cdc42; congenital heart disease; non-muscle myosin; zipper Drosophila; cardiogenesis; morphogenesis; tinman; Cdc42; congenital heart disease; non-muscle myosin; zipper

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Vogler, G.; Bodmer, R. Cellular Mechanisms of Drosophila Heart Morphogenesis. J. Cardiovasc. Dev. Dis. 2015, 2, 2-16.

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