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*
Hanson Center for Cancer Research, Adelaide, South Australia;
Department of Biochemistry and Biophysics, Washington State University, Pullman, WA 99164; and
Division of Biochemistry and Molecular Biology, John Curtin School of Medical Research, Australian National University, Canberra, Australia
The high-mobility group I(Y) (HMGI(Y)) family of proteins plays an
important architectural role in chromatin and have been implicated in
the control of inducible gene expression. We have previously shown that
expression of HMGI antisense RNA in Jurkat T cells inhibits the
activity of the IL-2 promoter. Here we have investigated the role of
HMGI(Y) in controlling IL-2 promoter-reporter constructs as well as the
endogenous IL-2 gene in both Jurkat T cells and human PBL. We found
that the IL-2 promoter has numerous binding sites for HMGI(Y), which
overlap or are adjacent to the known transcription factor binding
sites. HMGI(Y) modulates binding to the IL-2 promoter of at least three
transcription factor families, AP-1, NF-AT and NF-
B. By using a
mutant HMGI that cannot bind to DNA but can still interact with the
transcription factors, we found that DNA binding by HMGI was not
essential for the promotion of transcription factor binding. However,
the non-DNA binding mutant acts as a dominant negative protein in
transfection assays, suggesting that the formation of functional
HMGI(Y)-containing complexes requires DNA binding as well as
protein:protein interactions. The alteration of HMGI(Y) levels affects
IL-2 promoter activity not only in Jurkat T cells but also in PBL.
Importantly, we also show here that expression of the endogenous IL-2
gene as well as proliferation of PBL are affected by changes in HMGI(Y)
levels. These results demonstrate a major role for HMGI(Y) in IL-2
expression and hence T cell proliferation.
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