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Originally published In Press as doi:10.1074/jbc.M200248200 on February 14, 2002

J. Biol. Chem., Vol. 277, Issue 17, 15053-15060, April 26, 2002
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Nuclear Import and Export Signals in Control of the p53-related Protein p73*

Tomomi Inoue, Jeremy Stuart, Richard Leno, and Carl G. MakiDagger

From the Harvard University School of Public Health, Department of Cancer Cell Biology, Boston, Massachusetts 02115

The p53-family of proteins, including p53, p63, and p73, shares a high degree of structural similarity and can carry out some redundant functions. However, mechanisms that regulate the localization and activity of these proteins have not been fully clarified. In this study, a nuclear localization signal (NLS) was identified in p73, which is required for p73 nuclear import and which could promote the nuclear import of a heterologous, cytoplasmic protein. Mutants lacking the NLS localized to the cytoplasm and displayed diminished transcriptional activity. A nuclear export signal (NES) was also recognized in p73s C terminus, the deletion of which caused p73 to display a more nuclear localization pattern. This NES was sensitive to leptomycin B and could function as an independent export signal when fused to a heterologous protein. Interestingly, p73 mutant proteins lacking the NLS or the NES were more stable than wild-type p73, suggesting that nuclear import and nuclear export are required for efficient p73 degradation. Our results indicate that p73 localization is controlled by both nuclear import and export and suggest that the overall distribution of p73 is likely to result from the balance between these two processes. Proper control of nuclear import and export is likely to be an important regulatory determinant of p73.

* This work was supported by NCI, National Institutes of Health Grant 1R01CA80918-01 and American Cancer Society Grant RSG-01-042-01 (to C. G. M.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger To whom correspondence should be addressed: Harvard University School of Public Health, Dept. of Cancer Cell Biology, 665 Huntington Ave., Bldg. 1, 4th Floor, Boston, MA 02115. Tel.: 617-432-2532; Fax: 617-432-0107; E-mail: cmaki@hsph.harvard.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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