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  • Original Paper
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B-MYB transactivates its own promoter through SP1-binding sites

Oncogene volume 18, pages 1333–1339 (1999)Cite this article

Abstract

B-MYB is an ubiquitous protein required for mammalian cell growth. In this report we show that B-MYB transactivates its own promoter through a 120 bp segment proximal to the transcription start site. The B-MYB-responsive element does not contain myb-binding sites and gel-shift analysis shows that SP1, but not B-MYB, protein contained in SAOS2 cell extracts binds to the 120 bp B-myb promoter fragment. B-MYB-dependent transactivation is cooperatively increased in the presence of SP1, but not SP3 overexpression. When the SP1 elements of the B-myb promoter are transferred in front of a heterologous promoter, an increased response to B-MYB results. In contrast, c-MYB, the prototype member of the Myb family, is not able to activate the luciferase construct containing the SP1 elements. With the use of an SP1-GAL4 fusion protein, we have determined that the cooperative activation occurs through the domain A of SP1. These observations suggest that B-MYB functions as a coactivator of SP1, and that diverse combinations of myb and SP1 sites may dictate the responsiveness of myb-target genes to the various members of the myb family.

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Acknowledgements

PDL is supported by the Associazione Italiana per la Ricerca sul Cancro. BS is on leave of absence from the Istituto di Biologia dello Sviluppo, CNR Palermo, Italy.

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Authors and Affiliations

  1. Department of Molecular Pharmacology and Pathology, Consorzio Mario Negri Sud, Via Nazionale 66030 S.Maria Imbaro (CH), Italy

    Arturo Sala & Maria N Cervellera

  2. Department of Microbiology-Immunology, Thomas Jefferson University, Kimmel Cancer Institute, 233S. 10th Street, Philadelphia, 19107, Pennsylvania, USA

    Cesare Peschle

  3. Department of Reumatology, 233S. 10th Street, Philadelphia, 19107, Pennsylvania, USA

    Biagio Saitta

  4. Department of Genetics, Molecular and General Biology, University of Naples `Federico II', via Mezzocannone 8, 80134, Naples, Italy

    Pasquale De Luca

  5. Eppley Cancer Institute, University of Nebraska Medical Center, Omaha, 68198, Nebraska, USA

    Robert E Lewis

  6. Ludwig Institute for Cancer Research, St. Mary's Hospital Medical School, London, W21PG, UK

    Roger Watson

  7. Laboratorio di Ematologia Oncologia Istituto Superiore di Sanita, Rome, Italy

    Ida Casella & Cesare Peschle

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  1. Arturo Sala
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Sala, A., Saitta, B., De Luca, P. et al. B-MYB transactivates its own promoter through SP1-binding sites. Oncogene 18, 1333–1339 (1999). https://doi.org/10.1038/sj.onc.1202421

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