Nucleic Acids Research, Vol 25, Issue 24 4921-4925, Copyright © 1997 by Oxford University Press
FC Lucibello, N Liu, J Zwicker, C Gross and R Muller
B- myb and cdc25C exemplify different groups of genes whose transcription
is consecutively up-regulated during the cell cycle. Both promoters are
controlled by transcriptional repression via modules consisting of an E2F
binding site (E2FBS) or the related CDE plus a contiguous CHR co-repressor
element. We now show that the B- myb repressor module, which is derepressed
early (mid G1), is preferentially recognized by E2F-DP complexes and that a
mutation selectively abolishing E2F binding impairs regulation. In
contrast, the cdc25C repressor module, which is derepressed late (S/G2),
interacts selectively with CDE-CHR binding factor-1 (CDF-1). E2F binding,
but not CDF-1 binding, requires specific nucleotides flanking the E2FBS/CDE
core, while CDF-1 binding, but not E2F binding, depends on specific
nucleotides in the CHR. Swapping these nucleotides between the two
promoters profoundly changes protein binding patterns and alters expression
kinetics. Thus predominant CDF-1 binding leads to derepression in late S,
predominant E2F binding results in up- regulation in late G1, while
promoters binding both E2F and CDF-1 with high efficiency show intermediate
kinetics. Our results support a model where the differential binding of E2F
and CDF-1 repressor complexes contributes to the timing of promoter
activity during the cell cycle.
ARTICLES
The differential binding of E2F and CDF repressor complexes contributes to the timing of cell cycle-regulated transcription
Institut fur Molekularbiologie und Tumorforschung (IMT), Philipps- Universitat Marburg, Emil-Mannkopff-Strasse 2, D-35033 Marburg, Germany.
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