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Development, Vol 122, Issue 12 3765-3773, Copyright © 1996 by Company of Biologists

JOURNAL ARTICLES

Notch signaling inhibits muscle cell differentiation through a CBF1-independent pathway

C Shawber, D Nofziger, JJ Hsieh, C Lindsell, O Bogler, D Hayward and G Weinmaster
Department of Biological Chemistry, UCLA School of Medicine, Los Angeles, CA 90095-1737, USA.

Notch controls cell fate by inhibiting cellular differentiation, presumably through activation of the transcriptional regulator human C promoter Binding Factor (CBF1), which transactivates the hairy and Enhancer of split (HES-1) gene. However, we describe constitutively active forms of Notch1, which inhibit muscle cell differentiation but do not interact with CBF1 or upregulate endogenous HES-1 expression. In addition, Jagged-Notch interactions that prevent the expression of muscle cell specific genes do not involve the upregulation of endogenous HES-1. In fact, exogenous expression of HES-1 in C2C12 myoblasts does not block myogenesis. Our data demonstrate the existence of a CBF1-independent pathway by which Notch inhibits differentiation. We therefore propose that Notch signaling activates at least two different pathways: one which involves CBF1 as an intermediate and one which does not.


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