Abstract
Congenital heart defects, clinically identified in both small and large animals, are multifactorial and complex. Although heritable factors are known to have a role in cardiovascular disease, the full genetic aetiology remains unclear. Model organism research has proven valuable in providing a deeper understanding of the essential factors in heart development. For example, mouse knock-out studies reveal a role for the Integrin adhesion receptor in cardiac tissue. Recent research in Drosophila melanogaster (the fruit fly), a powerful experimental model, has demonstrated that the link between the extracellular matrix and the cell, mediated by Integrins, is required for multiple aspects of cardiogenesis. Here we test the hypothesis that Integrins signal to the heart cells through Src42A kinase. Using the powerful genetics and cell biology analysis possible in Drosophila, we demonstrate that Src42A acts in early events of heart tube development. Careful examination of mutant heart tissue and genetic interaction data suggests that Src42A’s role is independent of Integrin and the Integrin-related Focal Adhesion Kinase. Rather, Src42A acts non-autonomously by promoting programmed cell death of the amnioserosa, a transient tissue that neighbors the developing heart.
Highlights
A properly functioning heart is intimately linked to its structure
Development of the heart can effectively be studied at the genetic level to reveal the genes that determine the identity of heart cells and that dictate the response of heart progenitors to signals from neighboring cells and tissues
Even in instances where a specific genetic factor has been correlated to heart development, it remains difficult to definitively establish a causal relationship and determine how this genetic abnormality contributes to disease [10]
Summary
A properly functioning heart is intimately linked to its structure. Defects in this structure may trigger immediate or later-onset heart disease. Development of the heart can effectively be studied at the genetic level to reveal the genes that determine the identity of heart cells and that dictate the response of heart progenitors to signals from neighboring cells and tissues. Clinical observations, especially those which involve domestic purebreds, suggest that the underlying cause of CHDs is often heritable [6,7]. Especially those which involve domestic purebreds, suggest that the underlying cause of CHDs is often heritable [6,7] This is supported by studies in the last fifteen years which have begun to link specific CHD’s to genetic aetiologies [8,9].
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