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A CDE/CHR‐like element mediates repression of transcription of the mouse RB2 (p130) gene
Author(s) -
Fajas Lluis,
Le Cam Laurent,
Polanowska Jolanta,
Fabbrizio Eric,
Servant Nadège,
Philips Alexandre,
Carnac Gilles,
Sardet Claude
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01363-6
Subject(s) - repressor , promoter , biology , transcription (linguistics) , microbiology and biotechnology , response element , gene , cyclin dependent kinase 1 , cyclin a , genetics , cell cycle , gene expression , cyclin , linguistics , philosophy
The bipartite repressor elements, termed cell cycle‐dependent element (CDE)/cell cycle regulatory element (CCRE)‐cell cycle homology region (CHR) control the growth‐dependent transcription of the cyclin A , cdc25C , cdc2 genes. Here, we have identified a functional element displaying the signature of the CDE–CHR in the promoter of the mouse RB2 (p130) gene, encoding the retinoblastoma protein family (pRB)‐related protein p130. This element locates close to the major transcription start site where it makes major groove contacts with proteins that can be detected in a cellular context using in vivo genomic footprinting techniques. Inactivation of either the CDE or CHR sequence strongly up‐regulates the p130 promoter activity in exponentially growing cells, a situation where endogenous p130 gene expression is almost undetectable. Electrophoretic mobility shift assays suggest that two different protein complexes bind independently to the p130 CDE and CHR elements, and that the protein(s) bound to the CDE might be related to those bound on cyclin A and cdc2 promoters.