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Genetic Deficiency of p38α Reveals its Critical Role in Myoblast Cell Cycle Exit:The p38α-JNK Connection

Eusebio Perdiguero, Vanessa Ruiz-Bonilla, Antonio L. Serrano and Pura Muñoz-Cánoves

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The regulation of skeletal muscle formation (myogenesis) is essential for normal development as well as in pathological conditions such as muscular dystrophies and inflammatory myopathies. Findings published over the past years have established a key role for the p38 MAP kinase signaling pathway in the control of muscle gene expression and myotube formation. However, the relative contribution of the four p38 MAP kinases (p38α, p38β, p38γ and p38δ) to this process was unknown. We have recently demonstrated that myoblasts lacking p38α, but not those lacking p38β or p38δ, were unable to differentiate and form multinucleated myotubes, while p38γ-deficient myoblasts exhibited an attenuated fusion capacity. Defective myogenesis in the absence of p38α was attributed to delayed cell cycle exit and continuous proliferation in differentiation-promoting conditions, caused by enhanced activation of the JNK/cJun pathway. We discuss these findings in the context of the emerging crosstalk of p38 and JNK signaling pathways in controlling cell growth and differentiation.

Authors

Eusebio Perdiguero

Center for Genomic Regulation, Barcelona, Spain

Vanessa Ruiz-Bonilla

Center for Genomic Regulation, Barcelona, Spain

Antonio L. Serrano

Center for Genomic Regulation, Barcelona, Spain

Pura Muñoz-Cánoves

Center for Genomic Regulation, Barcelona, Spain

Purchase article for $19

Subscribe to this journal for $129/year