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RESEARCH PAPER
1 Department of Pathology, New York University Cancer Institute, New York University School of Medicine, New York, New York 10016, USA; 2 School of Computer Science, Tel-Aviv University, Tel-Aviv 69978, Israel; 3 Skirball Institute of Biomolecular Medicine, New York University, New York, New York 10016, USA
We have combined genome-wide transcription factor binding and expression profiling to assemble a regulatory network controlling the myogenic differentiation program in mammalian cells. We identified a cadre of overlapping and distinct targets of the key myogenic regulatory factors (MRFs)—MyoD and myogenin—and Myocyte Enhancer Factor 2 (MEF2). We discovered that MRFs and MEF2 regulate a remarkably extensive array of transcription factor genes that propagate and amplify the signals initiated by MRFs. We found that MRFs play an unexpectedly wide-ranging role in directing the assembly and usage of the neuromuscular junction. Interestingly, these factors also prepare myoblasts to respond to diverse types of stress. Computational analyses identified novel combinations of factors that, depending on the differentiation state, might collaborate with MRFs. Our studies suggest unanticipated biological insights into muscle development and highlight new directions for further studies of genes involved in muscle repair and responses to stress and damage.
[Keywords: ChIP-on-chip; myogenesis; transcriptional regulation network]
Received November 18, 2004; revised version accepted January 13, 2005.
Article published online ahead of print. Article and publication date are at http://www.genesdev.org/cgi/doi/10.1101/gad.1281105.
4 Corresponding author.
E-MAIL brian.dynlacht{at}med.nyu.edu; FAX (212) 263-6157.
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