Nucleic Acids Research, 2002, Vol. 30, No. 8 1767-1773
© 2002 Oxford University Press
Oct-2 regulates CD36 gene expression via a consensus octamer, which excludes the co-activator OBF-1
School of Biological Sciences, University of Manchester, 2.205, Stopford Building, Oxford Road, Manchester M13 9PT, UK and 1Division of Molecular Immunology, The Walter and Eliza Hall Institute of Medical Research, PO Royal Melbourne Hospital, Victoria 3050, Australia
The POU domain transcription factor, Oct-2, is essential for the B cell-specific expression of CD36 in mouse B cells. In order to determine how Oct-2 mediates expression of CD36 in B cells, we cloned and analysed the mouse CD36 promoter. In contrast to the human CD36 promoter, the mouse promoter contains a consensus octamer element of the type ATGCTAAT. This octamer element can be bound by either Oct-1 or Oct-2 but requires the expression of Oct-2 to activate transcription in B cells. Mutation of the octamer element renders the CD36 promoter refractory to activation by Oct-2. Furthermore, we demonstrate that the CD36 octamer element does not support recruitment of the B cell-specific co-activator OBF-1 and that CD36 expression is unaffected in primary B cells derived from obf-1–/– mice. We conclude that Oct-2 activates CD36 gene expression in mouse B cells via the octamer element in the promoter. Our data also demonstrate that CD36 is the first example of an Oct-2-dependent gene whose expression in B cells is independent of OBF-1. These findings support the notion that Oct-2 regulates gene transcription by both OBF-1-dependent and -independent mechanisms.
* To whom correspondence should be addressed. Tel: +44 161 275 5978; Fax: +44 161 275 5082; Email: paul.shore{at}man.ac.uk
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