cardiac deletion of smyd2 is dispensable for mouse heart development心脏删除smyd2是可有可无的老鼠心脏的发展.pdfVIP

Cardiac Deletion of Smyd2 Is Dispensable for Mouse Heart Development 1. 2.¤ 1 1 Florian Diehl , Mark A. Brown , Machteld J. van Amerongen , Tatyana Novoyatleva , Astrid 1 2 4 ¨ 1 3 2 Wietelmann , June Harriss , Fulvia Ferrazzi , Thomas Bottger , Richard P. Harvey , Philip W. Tucker , Felix B. Engel1* 1 Department of Cardiac Development and Remodeling, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Hessen, Germany, 2 Section of Molecular Genetics and Microbiology and Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, Texas, United States of America, 3 Developmental Biology ` Division, Victor Chang Cardiac Research Institute, Darlinghurst, New South Wales, Australia, 4 Dipartimento di Informatica e Sistemistica, Universita degli Studi di Pavia, Pavia, Lombardia, Italia Abstract Chromatin modifying enzymes play a critical role in cardiac differentiation. Previously, it has been shown that the targeted deletion of the histone methyltransferase, Smyd1, the founding member of the SET and MYND domain containing (Smyd) family, interferes with cardiomyocyte maturation and proper formation of the right heart ventricle. The highly related paralogue, Smyd2 is a histone 3 lysine 4- and lysine 36-specific methyltransferase expressed in heart and brain. Here, we report that Smyd2 is differentially expressed during cardiac development with highest expression in the neonatal heart. To elucidate