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Title: Opposite roles of MRF4 and MyoD in cell proliferation and myogenic differentiation

Journal Article · · Biochemical and Biophysical Research Communications
 [1]; ; ; ; ;  [1];  [1]; ; ;  [2];  [1];  [3];  [4];  [2]
  1. Division of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul (Korea, Republic of)
  2. Division of Animal Biotechnology, School of Agricultural Biotechnology, Seoul National University, Seoul (Korea, Republic of)
  3. College of Agriculture, Yanbian University, Longjing (China)
  4. School of Biology and Food Engineering, Dalian Polytechnic University, Dalian (China)

The basic helix-loop-helix myogenic regulatory factors play critical roles in skeletal myogenesis. Among the myogenic regulatory factors (MRFs), MRF4 shows a biphasic expression pattern during the formation of myotomes, although its function remains unclear. In this study, we used BEF (spontaneously immortalized bovine embryonic fibroblast that shows myogenic differentiation by overexpression of MyoD) and C2C12 cells to investigate the function of MRF4. Ectopic expressions of MRF4 did not stimulate myogenic differentiation in the BEF and C2C12 cells, but did show a marked increase of cell proliferation, upregulation of cyclin E, and downregulation of p21{sup WAF1}. Furthermore, MRF4 was found to induce degradation of the MyoD protein, which acts as a transcriptional activator for p21{sup WAF1}, and thus indicates that MRF4 accelerates cell proliferation by suppressing MyoD-dependent p21{sup WAF1} expression. However, forced expression of MyoD in the MRF4-overexpressing cells inhibited cell proliferation and partially induced myogenic differentiation, which suggests that MyoD is a potential negative intercessor of MRF4 in the regulation of the cell cycle. Taken together, these results indicate that MRF4 and MyoD play competitive roles in myogenesis by stimulating cell proliferation and differentiation, respectively.

OSTI ID:
21033013
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 364, Issue 3; Other Information: DOI: 10.1016/j.bbrc.2007.10.042; PII: S0006-291X(07)02175-4; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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