Eya protein phosphatase activity regulates Six1–Dach–Eya transcriptional effects in mammalian organogenesis

Xue Li (), Kenneth A. Ohgi, Jie Zhang, Anna Krones, Kevin T. Bush, Christopher K. Glass, Sanjay K. Nigam, Aneel K. Aggarwal, Richard Maas, David W. Rose and Michael G. Rosenfeld ()
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Xue Li: School and Department of Medicine, UCSD
Kenneth A. Ohgi: School and Department of Medicine, UCSD
Jie Zhang: School and Department of Medicine, UCSD
Anna Krones: School and Department of Medicine, UCSD
Kevin T. Bush: School and Department of Medicine, UCSD
Christopher K. Glass: School and Department of Medicine, UCSD
Sanjay K. Nigam: School and Department of Medicine, UCSD
Aneel K. Aggarwal: Mount Sinai School of Medicine
Richard Maas: Brigham and Women's Hospital/Harvard Medical School
David W. Rose: University of California
Michael G. Rosenfeld: School and Department of Medicine, UCSD

Nature, 2003, vol. 426, issue 6964, 247-254

Abstract: Abstract The precise mechanistic relationship between gene activation and repression events is a central question in mammalian organogenesis, as exemplified by the evolutionarily conserved sine oculis (Six), eyes absent (Eya) and dachshund (Dach) network of genetically interacting proteins. Here, we report that Six1 is required for the development of murine kidney, muscle and inner ear, and that it exhibits synergistic genetic interactions with Eya factors. We demonstrate that the Eya family has a protein phosphatase function, and that its enzymatic activity is required for regulating genes encoding growth control and signalling molecules, modulating precursor cell proliferation. The phosphatase function of Eya switches the function of Six1–Dach from repression to activation, causing transcriptional activation through recruitment of co-activators. The gene-specific recruitment of a co-activator with intrinsic phosphatase activity provides a molecular mechanism for activation of specific gene targets, including those regulating precursor cell proliferation and survival in mammalian organogenesis.

Date: 2003
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DOI: 10.1038/nature02083

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