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Piven O.O.,Institute of Molecular Biology and Genetic | Kostetskii I.E.,Institute of Molecular Biology and Genetic | Macewicz L.L.,Institute of Molecular Biology and Genetic | Kolomiets Y.M.,Institute of Molecular Biology and Genetic | And 2 more authors.
Experimental Biology and Medicine | Year: 2011

Cell adhesion, mediated by N-cadherin, is critical for embryogenesis since N-cadherin-null embryos die during mid-gestation with multiple developmental defects. To investigate the role of N-cadherin in heart muscle development, N-cadherin was specifically deleted from myocardial cells in mice. The structural integrity of the myocardial cell wall was compromised in the N-cadherin mutant embryos, leading to a malformed heart and a delay in embryonic development. In contrast, cardiac-specific deletion of αE-catenin, found in adherens junctions, or β-catenin, did not cause any morphological defects in the embryonic heart, presumably due to compensation by αT-catenin that is normally found in intercalated disks and γ-catenin (plakoglobin), respectively. Embryos lacking β-catenin in the heart also exhibited a cardiac defect, but only later in development resulting in partial lethality. These genetic studies underscore the importance of the N-cadherin/catenin complex in cardiogenesis. © 2011 by the Society for Experimental Biology and Medicine. Source

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