MIM/BEG4, a Sonic hedgehog-responsive gene that potentiates Gli-dependent transcription

  1. Christopher A. Callahan1,2,
  2. Tyler Ofstad1,
  3. Lily Horng1,
  4. Jordon K. Wang1,
  5. Hanson H. Zhen1,
  6. Pierre A. Coulombe3, and
  7. Anthony E. Oro1,4
  1. 1Program in Epithelial Biology and 2Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA; 3Department of Biological Chemistry and Department of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

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.

Keywords

Footnotes

  • Supplemental material is available at http://www.genesdev.org.

  • Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1221804.

  • ↵4 Corresponding author. E-MAIL Oro{at}cmgm.stanford.edu; FAX (650) 723-8762.

    • Accepted September 14, 2004.
    • Received May 14, 2004.
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  1. doi: 10.1101/gad.1221804 Genes & Dev. 18: 2724-2729 Cold Spring Harbor Laboratory Press

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