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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oai:doaj.org-article:f8f389f43c3d47fb8b3b93fde593929d2021-11-25T06:25:22ZCardiac deletion of Smyd2 is dispensable for mouse heart development.1932-620310.1371/journal.pone.0009748https://doaj.org/article/f8f389f43c3d47fb8b3b93fde593929d2010-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20305823/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Chromatin 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.Florian DiehlMark A BrownMachteld J van AmerongenTatyana NovoyatlevaAstrid WietelmannJune HarrissFulvia FerrazziThomas BöttgerRichard P HarveyPhilip W TuckerFelix B EngelPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 3, p e9748 (2010) |
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Medicine R Science Q Florian Diehl Mark A Brown Machteld J van Amerongen Tatyana Novoyatleva Astrid Wietelmann June Harriss Fulvia Ferrazzi Thomas Böttger Richard P Harvey Philip W Tucker Felix B Engel Cardiac deletion of Smyd2 is dispensable for mouse heart development. |
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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. |
format |
article |
author |
Florian Diehl Mark A Brown Machteld J van Amerongen Tatyana Novoyatleva Astrid Wietelmann June Harriss Fulvia Ferrazzi Thomas Böttger Richard P Harvey Philip W Tucker Felix B Engel |
author_facet |
Florian Diehl Mark A Brown Machteld J van Amerongen Tatyana Novoyatleva Astrid Wietelmann June Harriss Fulvia Ferrazzi Thomas Böttger Richard P Harvey Philip W Tucker Felix B Engel |
author_sort |
Florian Diehl |
title |
Cardiac deletion of Smyd2 is dispensable for mouse heart development. |
title_short |
Cardiac deletion of Smyd2 is dispensable for mouse heart development. |
title_full |
Cardiac deletion of Smyd2 is dispensable for mouse heart development. |
title_fullStr |
Cardiac deletion of Smyd2 is dispensable for mouse heart development. |
title_full_unstemmed |
Cardiac deletion of Smyd2 is dispensable for mouse heart development. |
title_sort |
cardiac deletion of smyd2 is dispensable for mouse heart development. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2010 |
url |
https://doaj.org/article/f8f389f43c3d47fb8b3b93fde593929d |
work_keys_str_mv |
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