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J. Biol. Chem., Vol. 277, Issue 7, 5187-5193, February 15, 2002
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From the Molecular Virology Section, Laboratory of Molecular
Microbiology, NIAID, National Institutes of Health,
Bethesda, Maryland 20892-0460
Human T-cell leukemia virus type I (HTLV-I) is
the causative agent for adult T-cell leukemia (ATL). Molecularly, ATL
cells have extensive aneugenic abnormalities that occur, at least in part, from cell cycle dysregulation by the HTLV-I-encoded Tax oncoprotein. Here, we compared six HTLV-I-transformed cells to Jurkat
and primary peripheral blood mononuclear cells (PBMC) in their
responses to treatment with microtubule inhibitors. We found that both Jurkat and PBMCs arrested efficiently in mitosis when treated
with nocodazole. By contrast, all six HTLV-I cells failed to arrest
comparably in mitosis, suggesting that ATL cells have a defect in the
mitotic spindle assembly checkpoint. Mechanistically, we observed that
in HTLV-I Tax-expressing cells human spindle assembly checkpoint
factors hsMAD1 and hsMAD2 were mislocated from the nucleus to the
cytoplasm. This altered localization of hsMAD1 and hsMAD2 correlated
with loss of mitotic checkpoint function and chemoresistance to
microtubule inhibitors.
Prevalent Loss of Mitotic Spindle Checkpoint in Adult T-cell
Leukemia Confers Resistance to Microtubule Inhibitors*
*
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.
To whom correspondence should be addressed: Molecular Virology
Section, Laboratory of Molecular Microbiology, NIAID, National Institutes of Health, Bldg. 4, Rm. 306, 9000 Rockville Pike, Bethesda, MD 20892-0460. Tel.: 301-496-6680; Fax: 301-480-3686; E-mail: kj7e@nih.gov.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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