Cell cycle-regulated repression of B-myb transcription: Cooperation of an E2F site with a contiguous corepressor element

被引:70
作者
Liu, NS [1 ]
Lucibello, FC [1 ]
Zwicker, J [1 ]
Engeland, K [1 ]
Muller, R [1 ]
机构
[1] UNIV MARBURG,INST MOL BIOL & TUMORFORSCH,D-35033 MARBURG,GERMANY
关键词
D O I
10.1093/nar/24.15.2905
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
B-myb belongs to a group of cell cycle genes whose transcription is repressed in G(0)/early G(1) through a binding site for the transcription factor E2F. Here, we show that the B-myb repressor element is specifically recognised by heterodimers consisting of DP-1 and E2F-1, E2F-3 or E2F-4. Surprisingly, EPF-mediated repression is dependent on a contiguous compressor element that resembles the CHR previously established as a compressor of the CDE in cell cycle genes derepressed in S/G(2), such as cyclin A, cdc2 and cdc25C. A factor binding to the B-myb CHR was identified in fractionated HeLa nuclear extract and found to interact with the minor groove, as previously shown by in vivo footprinting for the cyclin A CHR. The B-myb and cdc25C CHRs are related with respect to protein binding but are functionally clearly distinct. Our results support a model where both E2F- and CDE-mediated repression, acting at different stages in the cell cycle, are dependent on promoter-specific CHR elements.
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收藏
页码:2905 / 2910
页数:6
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