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Nucleic Acids Research Advance Access published online on September 25, 2009
Nucleic Acids Research, doi:10.1093/nar/gkp773
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© The Author(s) 2009. Published by Oxford University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene Regulation, Chromatin and Epigenetics

SMYD1, the myogenic activator, is a direct target of serum response factor and myogenin

Dali Li1,2,*, Zhiyv Niu3, Weishi Yu1, Yu Qian1, Qian Wang1, Qiang Li2, Zhengfang Yi1, Jian Luo1, Xiushan Wu2, Yuequn Wang2, Robert J. Schwartz3 and Mingyao Liu1,3

1The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, 2College of Life Sciences, Hunan Normal University, Changsha, Hunan 410081, China and 3Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, TX 77030, USA

*To whom correspondence should be addressed. Tel: +86 21 5434 5016; Fax: +86 21 5434 4922; Email: dlli{at}bio.ecnu.edu.cn

Received May 13, 2009. Revised August 10, 2009. Accepted September 2, 2009.

SMYD1 is a heart and muscle specific SET-MYND domain containing protein, which functions as a histone methyltransferase and regulates downstream gene transcription. We demonstrated that the expression of SMYD1 is restricted in the heart and skeletal muscle tissues in human. To reveal the regulatory mechanisms of SMYD1 expression during myogenesis and cardiogenesis, we cloned and characterized the human SMYD1 promoter, which contains highly conserved serum response factor (SRF) and myogenin binding sites. Overexpression of SRF and myogenin significantly increased the endogenous expression level of Smyd1 in C2C12 cells, respectively. Deletion of Srf in the heart of mouse embryos dramatically decreased the expression level of Smyd1 mRNA and the expression of Smyd1 can be rescued by exogenous SRF introduction in SRF null ES cells during differentiation. Furthermore, we demonstrated that SRF binds to the CArG site and myogenin binds to the E-box element on Smyd1 promoter region using EMSA and ChIP assays. Moreover, forced expression of SMYD1 accelerates myoblast differentiation and myotube formation in C2C12 cells. Taken together, these studies demonstrated that SMYD1 is a key regulator of myogenic differentiation and acts as a downstream target of muscle regulatory factors, SRF and myogenin.


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