Increased proteolytic processing of full-length Gli2 transcription factor reduces the hedgehog pathway activity in vivo. Academic Article uri icon

Overview

MeSH

  • Animals
  • Cells, Cultured
  • Down-Regulation
  • Embryo, Mammalian
  • Female
  • Gene Expression Regulation, Developmental
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Protein Isoforms
  • Protein Structure, Tertiary
  • Signal Transduction
  • Transcription Factors
  • Up-Regulation

MeSH Major

  • Hedgehog Proteins
  • Kruppel-Like Transcription Factors
  • Protein Processing, Post-Translational

abstract

  • The proteolytic processing of Gli2 and Gli3 full-length transcription factors into repressors is a key step of the regulation in Hedgehog (Hh) signaling. The differential Gli2 and Gli3 processing is controlled by the processing determinant domain or PDD, but its significance is not clear. We generated a Gli2 mutant allele, Gli2(3PDD) , in which the Gli3PDD substitutes for the Gli2PDD. As expected, Gli2(3PDD) is processed more efficiently and at a different position as compared to Gli2, indicating that PDD also determines the extent and site of Gli2 and Gli3 processing in vivo. The increase in levels of the Gli2 repressor in Gli2(3PDD) mutant reduces the Hh pathway activity. Gli2(3PDD) processing is still regulated by Hh signaling. These results indicate that the proper balance between the Gli2 full-length activator and repressor is essential for Hh signaling. Copyright © 2011 Wiley-Liss, Inc.

publication date

  • April 2011

has subject area

  • Animals
  • Cells, Cultured
  • Down-Regulation
  • Embryo, Mammalian
  • Female
  • Gene Expression Regulation, Developmental
  • Hedgehog Proteins
  • Kruppel-Like Transcription Factors
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Protein Isoforms
  • Protein Processing, Post-Translational
  • Protein Structure, Tertiary
  • Signal Transduction
  • Transcription Factors
  • Up-Regulation

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed Central ID

  • PMC3071291

Digital Object Identifier (DOI)

  • 10.1002/dvdy.22578

PubMed ID

  • 21337666

Additional Document Info

start page

  • 766

end page

  • 774

volume

  • 240

number

  • 4