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Yeast Los1p has properties of an exportin-like nucleocytoplasmic transport factor for tRNA

Saccharomyces cerevisiae Los1p, which is genetically linked to the nuclear pore protein Nsp1p and several tRNA biogenesis factors, was recently grouped into the family of importin/karyopherin-β-like proteins on the basis of its sequence similarity. In a two-hybrid screen, we identified Nup2p as a nu...

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Bibliographic Details
Main Authors: Hellmuth, Klaus (Author) , Lau, Denise (Author) , Bischoff, F. Ralf (Author) , Künzler, Markus (Author) , Hurt, Ed (Author) , Simos, Geōrgios (Author)
Format: Article (Journal)
Language:English
Published: Nov. 1998
In: Molecular and cellular biology
Year: 1998, Volume: 18, Issue: 11, Pages: 6374-6386
ISSN:1098-5549
DOI:10.1128/MCB.18.11.6374
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1128/MCB.18.11.6374
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Author Notes:Klaus Hellmuth, Denise M. Lau, F. Ralf Bischoff, Markus Künzler, Ed Hurt, and George Simos
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Summary:Saccharomyces cerevisiae Los1p, which is genetically linked to the nuclear pore protein Nsp1p and several tRNA biogenesis factors, was recently grouped into the family of importin/karyopherin-β-like proteins on the basis of its sequence similarity. In a two-hybrid screen, we identified Nup2p as a nucleoporin interacting with Los1p. Subsequent purification of Los1p from yeast demonstrates its physical association not only with Nup2p but also with Nsp1p. By the use of the Gsp1p-G21V mutant, Los1p was shown to preferentially bind to the GTP-bound form of yeast Ran. Furthermore, overexpression of full-length or N-terminally truncated Los1p was shown to have dominant-negative effects on cell growth and different nuclear export pathways. Finally, Los1p could interact with Gsp1p-GTP, but only in the presence of tRNA, as revealed in an indirect in vitro binding assay. These data confirm the homology between Los1p and the recently identified human exportin for tRNA and reinforce the possibility of a role for Los1p in nuclear export of tRNA in yeast.
Item Description:Elektronische Reproduktion der Druck-Ausgabe 28. März 2023
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Physical Description:Online Resource
ISSN:1098-5549
DOI:10.1128/MCB.18.11.6374

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