Abstract
cdc2 gene expression is under the control of multiple factors. Although E2F/DP proteins have been reported to play a central role, they cannot account for all aspects of the fine modulation of cdc2 gene expression during cell cycle and embryonic development. To characterize the transcription factors that control cdc2 gene expression during nerve cell differentiation in avians, we have previously cloned the quail cdc2 gene promoter region. We had identified an octamer (CAGGTGGC) containing an E-box, which has important activity in regulating cdc2 transcription. Using in vivo genomic footprinting experiments, we show here that this motif, currently named IG, is the target of binding proteins at different stages of neuroretina development, confirming its importance as a regulatory response element for cdc2 gene expression. A subset of Helix – Loop – Helix family of transcription factors, known as Upstream Stimulatory Factors (USFs) specifically bind to this sequence as dimers. Moreover, our results indicate that USFs transactivate the promoter of cdc2 via the IG motif. These data may help to better understand the mechanisms that control cell division in differentiating nerve cells.
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Acknowledgements
We are grateful to Dr C Sardet and L Le Cam (IGM, Montpellier, France) for having initiated us to in vivo footprinting. We are indebted to Dr S Vaulon and her colleagues (INSERM U 129, Paris) for the USF1−/− mouse. We also would like to thank Dr E Derrington and Dr E Goillot (ENS, Lyon) for critical reading of the manuscript. Dr P Hainaut (IARC, Lyon) has to be thanked for his constant support. This work was supported by grants from the Association pour la Recherche contre le Cancer (ARC), the Lique Nationale contre le Cancer, the Retina France Association, and the Centre National de la Recherche Scientifique (CNRS).
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North, S., Espanel, X., Bantignies, F. et al. Regulation of cdc2 gene expression by the upstream stimulatory factors (USFs). Oncogene 18, 1945–1955 (1999). https://doi.org/10.1038/sj.onc.1202506
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DOI: https://doi.org/10.1038/sj.onc.1202506
