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          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Publikationen des W. G. Kerckhoff-Instituts     Display Documents



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ID: 559736.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Publikationen des W. G. Kerckhoff-Instituts
Cardiac deletion of Smyd2 is dispensable for mouse heart development
Authors:Diehl, F.; Brown, M. A.; van Amerongen, M. J.; Novoyatleva, T.; Wietelmann, A.; Harriss, J.; Ferrazzi, F.; Bottger, T.; Harvey, R. P.; Tucker, P. W.; Engel, F. B.
Title of Journal:PLoS ONE
Volume:5
Issue / Number:3
Start Page:e9748
Audience:Not Specified
Abstract / Description: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 the functional role of Smyd2 in the heart, we generated conditional knockout (cKO) mice harboring a cardiomyocyte-specific deletion of Smyd2 and performed histological, functional and molecular analyses. Unexpectedly, cardiac deletion of Smyd2 was dispensable for proper morphological and functional development of the murine heart and had no effect on global histone 3 lysine 4 or 36 methylation. However, we provide evidence for a potential role of Smyd2 in the transcriptional regulation of genes associated with translation and reveal that Smyd2, similar to Smyd3, interacts with RNA Polymerase II as well as to the RNA helicase, HELZ.
Free Keywords:Alleles; Animals; Brain/metabolism; *Gene Deletion; *Gene Expression Regulation, Developmental; Heart/*physiology; Histone-Lysine N-Methyltransferase/*genetics/*physiology; Mice; Mice, Inbred C57BL; Mice, Knockout; Myocardium/metabolism; RNA Helicases/metabolism; RNA Polymerase II/metabolism; Rats; Rats, Sprague-Dawley
External Publication Status:published
Document Type:Article
Version Comment:Automatic journal name synchronization
Communicated by:N. N.
Affiliations:MPI für physiologische und klinische Forschung
External Affiliations:Department of Cardiac Development and Remodeling, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Hessen, Germany.
Identifiers:ISSN:1932-6203 (Electronic) 1932-6203 (Linking)
URL:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=..
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