B-MYB transactivates its own promoter through SP1-binding sites

Arturo Sala, Biagio Saitta, Pasquale De Luca, Maria N. Cervellera, Ida Casella, Robert E Lewis, Roger Watson, Cesare Peschle

Research output: Contribution to journalArticle

37 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)1333-1339
Number of pages7
JournalOncogene
Volume18
Issue number6
DOIs
StatePublished - Feb 11 1999

Fingerprint

myb Genes
Binding Sites
Transcription Initiation Site
Electrophoretic Mobility Shift Assay
Cell Extracts
Luciferases
Transcriptional Activation
Proteins
Growth
IgA receptor

Keywords

  • B-MYB
  • Cell-cycle
  • Promoter
  • SP1
  • Transcription

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

Cite this

Sala, A., Saitta, B., De Luca, P., Cervellera, M. N., Casella, I., Lewis, R. E., ... Peschle, C. (1999). B-MYB transactivates its own promoter through SP1-binding sites. Oncogene, 18(6), 1333-1339. https://doi.org/10.1038/sj.onc.1202421

B-MYB transactivates its own promoter through SP1-binding sites. / Sala, Arturo; Saitta, Biagio; De Luca, Pasquale; Cervellera, Maria N.; Casella, Ida; Lewis, Robert E; Watson, Roger; Peschle, Cesare.

In: Oncogene, Vol. 18, No. 6, 11.02.1999, p. 1333-1339.

Research output: Contribution to journalArticle

Sala, A, Saitta, B, De Luca, P, Cervellera, MN, Casella, I, Lewis, RE, Watson, R & Peschle, C 1999, 'B-MYB transactivates its own promoter through SP1-binding sites', Oncogene, vol. 18, no. 6, pp. 1333-1339. https://doi.org/10.1038/sj.onc.1202421
Sala A, Saitta B, De Luca P, Cervellera MN, Casella I, Lewis RE et al. B-MYB transactivates its own promoter through SP1-binding sites. Oncogene. 1999 Feb 11;18(6):1333-1339. https://doi.org/10.1038/sj.onc.1202421
Sala, Arturo ; Saitta, Biagio ; De Luca, Pasquale ; Cervellera, Maria N. ; Casella, Ida ; Lewis, Robert E ; Watson, Roger ; Peschle, Cesare. / B-MYB transactivates its own promoter through SP1-binding sites. In: Oncogene. 1999 ; Vol. 18, No. 6. pp. 1333-1339.
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