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Molecular and Cellular Biology, December 2000, p. 8767-8782, Vol. 20, No. 23
0270-7306/00/$04.00+0

Mex67p of Schizosaccharomyces pombe Interacts with Rae1p in Mediating mRNA Export

Jin Ho Yoon,1 Dona C. Love,2 Anjan Guhathakurta,1 John A. Hanover,2 and Ravi Dhar1,*

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 (Delta 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 Delta 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.

Molecular and Cellular Biology, December 2000, p. 8767-8782, Vol. 20, No. 23
0270-7306/00/$04.00+0


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