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Analysis of the Bruton's tyrosine kinase gene promoter reveals critical
PU.1 and SP1 sites
A Himmelmann, C Thevenin, K Harrison and JH Kehrl
Laboratory of Immunoregulation, National Institute of Allergy and
Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-
1876, USA.
The gene defective in X-linked agammaglobulinemia (XLA) encodes a novel
protein kinase termed Bruton's tyrosine kinase (Btk). Whereas the XLA
phenotype is confined to abnormalities of B-cell development and function,
Btk is expressed not only in B-lymphocyte lineage but also in myeloid
lineage cells. The first 450 basepairs of the Btk promoter fused to a
luciferase gene displayed a similar cell-type specificity. Critical binding
sites for the transcription factors PU.1 and Sp1 were identified in the
proximal portion of the Btk promoter upstream of a cluster of
transcriptional start sites. Mutation of either the PU.1 or Sp1 site
markedly reduced the activity of a Btk promoter-luciferase reporter
construct in transfection experiments. In addition, PU.1 directly
transactivated the Btk promoter, and deletion of the PU.1 binding site
abolished this effect. This study implicates PU.1 and Sp1 as major
regulators of Btk expression and provides a foundation for further study of
the regulation of this gene in XLA patients that lack Btk mRNA.
Volume 87,
Issue 3,
pp. 1036-1044,
02/01/1996
Copyright © 1996 by The American Society of Hematology
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