Cardiac deletion of Smyd2 is dispensable for mouse heart development

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...

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Bibliographic Details
Published in:PloS one 2010-03, Vol.5 (3), p.e9748
Main Authors: Diehl, Florian, Brown, Mark A, van Amerongen, Machteld J, Novoyatleva, Tatyana, Wietelmann, Astrid, Harriss, June, Ferrazzi, Fulvia, Böttger, Thomas, Harvey, Richard P, Tucker, Philip W, Engel, Felix B
Format: Article
Language:English
Subjects:
Alleles
Animals
Brain
Brain - metabolism
Cardiomyocytes
Cardiomyopathy
Cell Biology/Gene Expression
Cell Biology/Nuclear Structure and Function
Cell cycle
Chromatin
Developmental biology
Developmental Biology/Cell Differentiation
Developmental Biology/Organogenesis
DNA helicase
DNA-directed RNA polymerase
Experiments
Gene Deletion
Gene expression
Gene Expression Regulation, Developmental
Gene regulation
Genes
Genomics
Heart
Heart - physiology
Heart diseases
Histone methyltransferase
Histone-Lysine N-Methyltransferase - genetics
Histone-Lysine N-Methyltransferase - physiology
Histones
Laboratory animals
Lysine
Metabolism
Methylation
Methyltransferases
Mice
Mice, Inbred C57BL
Mice, Knockout
Molecular biology
Myocardium - metabolism
Neonates
Proteins
Rats
Rats, Sprague-Dawley
Ribonucleic acid
RNA
RNA helicase
RNA Helicases - metabolism
RNA polymerase II
RNA Polymerase II - metabolism
Rodents
Transcription
Transcription (Genetics)
Translation (Genetics)
Ventricle
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Summary: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.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0009748