MyoD induces the expression of p57Kip2 in cells lacking p21Cip1/Waf1: Overlapping and distinct functions of the two cdk inhibitors

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, t...

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Bibliographic Details
Published in:Journal of cellular physiology 2004-09, Vol.200 (3), p.468-475
Main Authors: Figliola, Rocco, Maione, Rossella
Format: Article
Language:English
Subjects:
3T3 Cells
Animals
Blotting, Western
Cell Line, Transformed
Cell Transformation, Viral
Cyclin-Dependent Kinases - metabolism
Cyclins - deficiency
Cyclins - genetics
Cyclins - metabolism
Cyclins - physiology
Fibroblasts - metabolism
Gene Expression Regulation, Developmental
Mice
Mice, Inbred BALB C
Mice, Inbred C3H
Mice, Knockout
MyoD Protein - genetics
MyoD Protein - physiology
NIH 3T3 Cells
Precipitin Tests
Retroviridae - genetics
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Summary: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.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.20044