Document Detail


Tandem E2F binding sites in the promoter of the p107 cell cycle regulator control p107 expression and its cellular functions.
MedLine Citation:
PMID:  20585628     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The retinoblastoma tumor suppressor (Rb) is a potent and ubiquitously expressed cell cycle regulator, but patients with a germline Rb mutation develop a very specific tumor spectrum. This surprising observation raises the possibility that mechanisms that compensate for loss of Rb function are present or activated in many cell types. In particular, p107, a protein related to Rb, has been shown to functionally overlap for loss of Rb in several cellular contexts. To investigate the mechanisms underlying this functional redundancy between Rb and p107 in vivo, we used gene targeting in embryonic stem cells to engineer point mutations in two consensus E2F binding sites in the endogenous p107 promoter. Analysis of normal and mutant cells by gene expression and chromatin immunoprecipitation assays showed that members of the Rb and E2F families directly bound these two sites. Furthermore, we found that these two E2F sites controlled both the repression of p107 in quiescent cells and also its activation in cycling cells, as well as in Rb mutant cells. Cell cycle assays further indicated that activation of p107 transcription during S phase through the two E2F binding sites was critical for controlled cell cycle progression, uncovering a specific role for p107 to slow proliferation in mammalian cells. Direct transcriptional repression of p107 by Rb and E2F family members provides a molecular mechanism for a critical negative feedback loop during cell cycle progression and tumorigenesis. These experiments also suggest novel therapeutic strategies to increase the p107 levels in tumor cells.
Authors:
Deborah L Burkhart; Stacey E Wirt; Anne-Flore Zmoos; Michael S Kareta; Julien Sage
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-06-24
Journal Detail:
Title:  PLoS genetics     Volume:  6     ISSN:  1553-7404     ISO Abbreviation:  PLoS Genet.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-06-29     Completed Date:  2010-09-27     Revised Date:  2011-03-11    
Medline Journal Info:
Nlm Unique ID:  101239074     Medline TA:  PLoS Genet     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e1001003     Citation Subset:  IM    
Affiliation:
Departments of Pediatrics and Genetics, Stanford Medical School, Stanford, California, United States of America.
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MeSH Terms
Descriptor/Qualifier:
Animals
Base Sequence
Binding Sites
Cell Cycle*
Cell Cycle Proteins
Cells, Cultured
Conserved Sequence
E2F Transcription Factors / metabolism*
Humans
Mice
Molecular Sequence Data
Promoter Regions, Genetic*
Retinoblastoma-Like Protein p107 / chemistry,  genetics,  metabolism*
Sequence Alignment
Transcription, Genetic
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/E2F Transcription Factors; 0/Rbl1 protein, mouse; 0/Retinoblastoma-Like Protein p107
Comments/Corrections

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