Yeast Genetics and Molecular Biology 2002
University of Wisconsin
Madison, Wisconsin USA
July 30 - August 4, 2002


Name: Ford, Amanda
Mailing Address: Molecular Biology and Genetics, University of Wisconsin, 1525 Linden Drive, Madison, WI 53706, USA
Email Address: asford@students.wisc.edu
Phone & FAX numbers: 608-262-4381 & 608-262-4570

Abstract #30


Session Title: Control Gene Regulators
Session Time: Thursday, August 1 -- 9:00AM - 10:30AM
Presentation: Platform
Topic: Gene Expression

Nuclear Import of Upf3p Is Mediated by Importin alpha/beta and Export of Upf3p is Required for a Functional NMD Pathway in Yeast.
Amanda Ford (1), Renee Shirley (1), M. Rachel Richards (1), Markus Albertini (2), Michael Culbertson (1)
(1) Molecular Biology and Genetics, University of Wisconsin, 1525 Linden Drive, Madison, WI 53706, USA; (2) Laboratory of Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, New York 10021.

Upf3p, which is required for nonsense-mediated mRNA decay (NMD) in yeast, is primarily cytoplasmic but accumulates inside the nucleus when UPF3 is over-expressed or when upf3 - mutations prevent nuclear export. Upf3p physically interacts with Srp1p (importin-alpha) and Upf3p fails to import into the nucleus in a temperature-sensitive srp1-31 strain. These data indicate that nuclear import is mediated by the importin alpha/beta heterodimer. Nuclear export of Upf3p is mediated by a leucine-rich nuclear export sequence (NES-A), but export is not dependent on the Crm1p exportin. Mutations identified in NES-A prevent nuclear export and confer a Nmd- phenotype. The addition of a functional NES element to an export-defective upf3- allele restores export and partially restores a Nmd+ phenotype. Our findings support a model in which the movement of Upf3p between the nucleus and the cytoplasm is required for a fully functional NMD pathway. We also found that over-expression of Upf2p suppresses the Nmd - phenotype in mutant strains carrying nes-A alleles but has no effect on the localization of Upf3p, indicating that the mutations in NES-A that impair nuclear export cause additional defects in the function of Upf3p that are not rectified by restoration of export alone. Our results suggest a model in which Upf3p functions in one of the initital steps leading to the rapid decay of mRNAs that cannot be translated full length during the first round of translation.


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