Document Detail


A Lin-9 complex is recruited by B-Myb to activate transcription of G2/M genes in undifferentiated embryonal carcinoma cells.
MedLine Citation:
PMID:  19252525     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
It has recently been discovered that cell-cycle gene transcription is regulated by a core complex named LINC that switches from a transcriptionally repressive complex in G(0)-G(1) with the p130 or p107 pocket proteins and E2F4 to a transcriptionally active complex in S-G(2) containing B-Myb. We have studied the function of LINC in F9 embryonal carcinoma cells, which are distinguished by a rapid cell cycle resulting from an extremely short G(1) phase. We show that suppressing expression of the LINC component, Lin-9, in F9 cells causes arrest in mitosis, and we have used this system to screen for transcriptional targets. In these cells, B-Myb was found in complexes with Lin-9 and several other LINC constituents, however, the pocket proteins did not associate with LINC unless F9 cells were differentiated. Lin-9 and B-Myb were both required for transcription of G(2)/M genes such as Cyclin B1 and Survivin. Moreover, B-Myb was demonstrated to recruit Lin-9 to the Survivin promoter through multiple Myb-binding sites. The demonstration that a B-Myb/LINC complex is vital for progression through mitosis in cells lacking a G(1)/S checkpoint has implications for both undifferentiated embryonal cells and for cancers in which pocket protein function is compromised.
Authors:
A S Knight; M Notaridou; R J Watson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-03-02
Journal Detail:
Title:  Oncogene     Volume:  28     ISSN:  1476-5594     ISO Abbreviation:  Oncogene     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-04-16     Completed Date:  2009-04-28     Revised Date:  2010-08-31    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  England    
Other Details:
Languages:  eng     Pagination:  1737-47     Citation Subset:  IM    
Affiliation:
Department of Virology, Faculty of Medicine, Imperial College London, London, UK.
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MeSH Terms
Descriptor/Qualifier:
Animals
Binding Sites
Cell Cycle Proteins / physiology*
Cell Division / genetics*
Chromatin Immunoprecipitation
Cyclin B / genetics
Cyclin B1
E2F Transcription Factors / physiology
Embryonal Carcinoma Stem Cells / metabolism*
G2 Phase / genetics*
Mice
Microtubule-Associated Proteins / genetics
Promoter Regions, Genetic
Trans-Activators / physiology*
Transcriptional Activation*
Tumor Suppressor Proteins / physiology*
Chemical
Reg. No./Substance:
0/Birc5 protein, mouse; 0/Ccnb1 protein, mouse; 0/Cell Cycle Proteins; 0/Cyclin B; 0/Cyclin B1; 0/E2F Transcription Factors; 0/LIN-9 protein, mouse; 0/Microtubule-Associated Proteins; 0/Mybl2 protein, mouse; 0/Trans-Activators; 0/Tumor Suppressor Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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