MyoD induces the expression of p57Kip2 in cells lacking p21Cip1/Waf1: Overlapping and distinct functions of the two cdk inhibitors
Article first published online: 17 FEB 2004
Copyright © 2004 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 200, Issue 3, pages 468–475, September 2004
How to Cite
Figliola, R. and Maione, R. (2004), MyoD induces the expression of p57Kip2 in cells lacking p21Cip1/Waf1: Overlapping and distinct functions of the two cdk inhibitors. J. Cell. Physiol., 200: 468–475. doi: 10.1002/jcp.20044
- Issue published online: 1 JUL 2004
- Article first published online: 17 FEB 2004
- Manuscript Accepted: 5 DEC 2003
- Manuscript Received: 6 OCT 2003
- Ministero dell'Istruzione, dell'Università e della Ricerca (MIUR). Grant Numbers: 2002055585_002, RBNE0132MY_001
- Consiglio Nazionale delle Ricerche (CNR). Grant Number: CNRC00A4F4_002
- Associazione Italiana per la Ricerca sul Cancro (AIRC). Grant Number: 1165
The myogenic factor MyoD induces the expression of the cdk inhibitor p21 to promote cell cycle withdrawal in differentiating myoblasts. Although the cdk inhibitor p57 is also highly expressed in skeletal muscle and is thought to redundantly control myogenesis, little is known about its regulation, that has been suggested to be independent of MyoD. Here we show, for the first time, that MyoD is capable to induce the expression of p57. Intriguingly, this ability is restricted to cells lacking p21, suggesting that the two cdk inhibitors may be expressed in different muscle cell lineages. We also suggest that the functions of p21 and p57 in myoblast cells are only in part redundant. In fact, while the two cdk inhibitors play a similar role in cells undergoing G1 arrest during MyoD-induced differentiation, p57 does not replace p21 in cells escaping G1 arrest and undergoing MyoD-induced apoptosis. This difference can be ascribed both to a different subcellular localization and to a differential ability of the two cdk inhibitors to interact with cell cycle regulators. © 2004 Wiley-Liss, Inc.