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Molecular and Cellular Biology, December 2000, p. 8767-8782, Vol. 20, No. 23
Basic Research Laboratory, National Cancer
Institute,1 and Laboratory of Cell
Biochemistry and Biology, National Institute of Diabetes and
Digestive and Kidney Diseases,2 National
Institutes of Health, Bethesda, Maryland 20892
Received 3 May 2000/Returned for modification 5 June 2000/Accepted 12 September 2000
We identified the Schizosaccharomyces pombe mex67 gene
(spmex67) as a multicopy suppressor of rae1-167
nup184-1 synthetic lethality and the rae1-167 ts
mutation. spMex67p, a 596-amino-acid-long protein, has
considerable sequence similarity to the Saccharomyces cerevisiae Mex67p (scMex67p) and human Tap. In contrast to
scMEX67, spmex67 is essential for neither
growth nor nuclear export of mRNA. However, an spmex67 null
mutation (
0270-7306/00/$04.00+0
Mex67p of Schizosaccharomyces pombe
Interacts with Rae1p in Mediating mRNA Export
mex67) is synthetically lethal with the
rae1-167 mutation and accumulates poly(A)+ RNA
in the nucleus. We identified a central region (149 to 505 amino acids)
within spMex67p that associates with a complex
containing Rae1p that complements growth and mRNA export defects of the
rae1-167
mex67 synthetic lethality. This region is
devoid of RNA-binding, N-terminal nuclear localization, and the
C-terminal nuclear pore complex-targeting regions. The (149-505)-green
fluorescent protein (GFP) fusion is found diffused throughout
the cell. Overexpression of spMex67p inhibits growth and mRNA
export and results in the redistribution of the diffused
localization of the (149-505)-GFP fusion to the nucleus and the
nuclear periphery. These results suggest that spMex67p competes for
essential mRNA export factor(s). Finally, we propose that the
149-505 region of spMex67p could act as an accessory
factor in Rae1p-dependent transport and that spMex67p participates
at various common steps with Rae1p export complexes in promoting the
export of mRNA.
*
Corresponding author. Mailing address: Basic Research
Laboratory, National Cancer Institute, National Institutes of Health, Bldg. 41, Rm. A222, 9000 Rockville Pike, Bethesda, MD 20892. Phone: (301) 496-0990. Fax: (301) 496-4951. E-mail:
dharr{at}dce41.nci.nih.gov.
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