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The zinc finger protein ZPR1 translocates from the cytoplasm to the
nucleus after treatment of cells with mitogens. The function of nuclear
ZPR1 has not been defined. Here we demonstrate that ZPR1 accumulates in
the nucleolus of proliferating cells. The role of ZPR1 was examined
using a gene disruption strategy. Cells lacking ZPR1 are not viable.
Biochemical analysis demonstrated that the loss of ZPR1 caused
disruption of nucleolar function, including preribosomal RNA
expression. These data establish ZPR1 as an essential protein that is
required for normal nucleolar function in proliferating cells.

Howard Hughes Medical Institute and
*Program in
Molecular Medicine, Department of Biochemistry and Molecular Biology,
University of Massachusetts Medical School, Worcester, Massachusetts
01605;
§Department of Biology, Assumption College,
Worcester, Massachusetts 01615;
Department of Molecular
and Experimental Medicine, The Scripps Research Institute, La Jolla,
California 92037; and
Department of Genetics, Harvard
Medical School, Boston Massachusetts 02115
Present address: Molecular Cardiology Research
Center, New England Medical Center, Boston, MA 02111.
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