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MOLECULAR AND CELLULAR BIOLOGY, Nov. 2002, p. 78687876 Vol. 22, No. 22 0270-7306/02/$04.00 0 DOI: 10.1128/MCB.22.22.78687876.2002
 

Summary: MOLECULAR AND CELLULAR BIOLOGY, Nov. 2002, p. 78687876 Vol. 22, No. 22
0270-7306/02/$04.00 0 DOI: 10.1128/MCB.22.22.78687876.2002
Copyright 2002, American Society for Microbiology. All Rights Reserved.
Role for the Mortality Factors MORF4, MRGX, and MRG15 in
Transcriptional Repression via Associations with Pf1,
mSin3A, and Transducin-Like Enhancer of Split
Gregory S. Yochum and Donald E. Ayer*
Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah,
Salt Lake City, Utah 84112-5550
Received 21 June 2002/Returned for modification 30 July 2002/Accepted 15 August 2002
mSin3A and Transducin-Like Enhancer of Split (TLE) are two histone deacetylase (HDAC)-containing
corepressors that function to repress transcription at targeted genes. Pf1 is a plant homeodomain zinc finger
protein that interacts with both mSin3A and TLE, suggesting that it coordinates their function. Here we show
that mSin3A and TLE interact with members of the mortality factor (MORF) family of putative transcriptional
regulators. This family comprises MORF on chromosome 4 (MORF4) and MORF-related genes on chromo-
somes X and 15 (MRGX and MRG15, respectively) and is proposed to contribute to cellular senescence.
Consistent with a role in transcription, we demonstrate that Gal4 fusions to each MORF family member
repress transcription from a Gal4-dependent luciferase reporter. By using both mapping experiments and a
dominant negative form of TLE, we show that repression by MORFs requires associations with mSin3A and
TLE. Therefore, common functions of the MORFs are likely elicited through the action of a MORF/mSin3A/

  

Source: Ayer, Don - Huntsman Cancer Institute, University of Utah

 

Collections: Biology and Medicine