期刊
NATURE CELL BIOLOGY
卷 8, 期 7, 页码 717-U143出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb1432
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- FIC NIH HHS [R01 TW06186-01] Funding Source: Medline
- Intramural NIH HHS Funding Source: Medline
Emerging evidence suggests that supernumerary centrosomes drive genome instability and oncogenesis(1-3). Human T-cell leukaemia virus type I ( HTLV-I) is etiologically associated with adult T-cell leukaemia ( ATL) 4. ATL cells are aneuploid, but the causes of aneuploidy are incompletely understood(5,6). Here, we show that centrosome amplification is frequent in HTLV-I-transformed cells and that this phenotype is caused by the viral Tax oncoprotein. We also show that the fraction of Tax protein that localizes to centrosomes interacts with TAX1BP2, a novel centrosomal protein composed almost entirely of coiled-coil domains. Overexpression of TAX1BP2 inhibited centrosome duplication, whereas depletion of TAX1BP2 by RNAi resulted in centrosome hyperamplification. Our findings suggest that the HTLV-I Tax oncoprotein targets TAX1BP2 causing genomic instability and aneuploidy.
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