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

Christopher A. Callahan, Tyler Ofstad, Lily Horng, Jordon K. Wang, Hanson H. Zhen, Pierre A. Coulombe, Anthony E. Oro

Research output: Contribution to journalArticlepeer-review

Abstract

Sonic hedgehog (Shh) signaling plays a critical role during development and carcinogens. 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.

Original languageEnglish (US)
Pages (from-to)2724-2729
Number of pages6
JournalGenes and Development
Volume18
Issue number22
DOIs
StatePublished - Nov 15 2004

Keywords

  • Actin
  • BCC
  • Gli
  • MIM
  • Sonic hedgehog
  • Transcription

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

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