CHD7 cooperates with PBAF to control multipotent neural crest formation

Ruchi Bajpai, Denise A. Chen, Alvaro Rada-Iglesias, Junmei Zhang, Yiqin Xiong, Jill Helms, Ching-Pin Chang, Yingming Zhao, Tomek Swigut and Joanna Wysocka ()
Additional contact information
Ruchi Bajpai: Department of Chemical and Systems Biology,
Denise A. Chen: Department of Chemical and Systems Biology,
Alvaro Rada-Iglesias: Department of Chemical and Systems Biology,
Junmei Zhang: Protein Chemistry Technology Center, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
Yiqin Xiong: Department of Medicine, Division of Cardiovascular Medicine,
Jill Helms: Department of Surgery,
Ching-Pin Chang: Department of Surgery,
Yingming Zhao: University of Chicago, Chicago, Illinois 60637, USA
Tomek Swigut: Department of Chemical and Systems Biology,
Joanna Wysocka: Department of Chemical and Systems Biology,

Nature, 2010, vol. 463, issue 7283, 958-962

Abstract: Neural crest abnormalities 'CHARGE syndrome' is a rare congenital condition characterized by malformations of the craniofacial structures, peripheral nervous system, ears, eyes and heart. It is caused by heterozygous mutations in the gene for CHD7, an ATP-dependent chromatin-remodelling protein. It was postulated 25 years ago that CHARGE syndrome results from the abnormal development of the neural crest. This hypothesis has remained untested, but Bajpai et al. now show that CHD7 is essential for the formation of multipotent migratory neural crest, and is essential for activating the neural crest transcriptional circuitry. In addition, CHD7 is shown to cooperate with another chromatin-remodelling complex, PBAF, to promote neural crest gene expression and cell migration.

Date: 2010
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DOI: 10.1038/nature08733

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