MIM/BEG4, a Sonic hedgehog-responsive gene that potentiates Gli-dependent transcription
Abstract
Sonic hedgehog (Shh) signaling plays a critical role during development and carcinogenesis. While Gli family members govern the transcriptional output of Shh signaling, little is known how Gli-mediated transcriptional activity is regulated. Here we identify the actin-binding protein Missing in Metastasis (MIM) as a new Shh-responsive gene. Together, Gli1 and MIM recapitulate Shh-mediated epidermal proliferation and invasion in regenerated human skin. MIM is part of a Gli/Suppressor of Fused complex and potentiates Gli-dependent transcription using domains distinct from those used for monomeric actin binding. These data define MIM as both a Shh-responsive gene and a new member of the pathway that modulates Gli responses during growth and tumorigenesis.
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Footnotes
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Supplemental material is available at http://www.genesdev.org.
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Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1221804.
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↵4 Corresponding author. E-MAIL Oro{at}cmgm.stanford.edu; FAX (650) 723-8762.
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- Accepted September 14, 2004.
- Received May 14, 2004.
- Cold Spring Harbor Laboratory Press