J. Biochem, 1999, Vol. 125, No. 3 574-585
© 1999 Japanese Biochemical Society
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Disruption of the YRB2 Gene Retards Nuclear Protein Export, Causing a Profound Mitotic Delay, and Can Be Rescued by Overexpression of XPO1/CRM11
*Department of Molecular Biology, Graduate School of Medical Science, Kyushu University 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582;
Verna and Marrs McLean Department of Biochemistry, Baylor College of Medicine One Baylor Plaza, Houston, Texas 77030, USA
2To whom correspondence should be addressed. Tel: +81-92-642-6175, Fax: +81-92-642-6183, E-mail:tnishi{at}molbiol.med.kyushu-u.ac.jp
Disruption of the YRB2 gene encoding a nuclear Ran-binding protein homologous to Yrb1p/RanBP1 makes Saccharomyces cerevisiae cold sensitive for colony-formation, but not for growth in liquid medium. Schizosaccharomyces pombe Hbalp, which is homologous to Saccharomyces cerevisiae Yrb2p, rescued the cold sensitivity of 
yrb2 cells. When released from an 
factor block, yrb2 cells underwent a prolonged delay at the short spindle stage of mitosis with a normal level of Clb/p34CDC28 kinase activity, but there was no chromosome loss, this being consistent with the finding that yrb2 was synthetic lethal with neither Arnadl nor mad3. The cold sensitive colony-formation of yrb2 cells was rescued by both XPO1/CRM1 and GSP1, but not CDC5, carried on a multicopy vector. XP01/CRM1 rescued yrb2 even in a single copy. Consistent with such a tight functional interaction, Xpo1p/Crm1p directly bound to Yrb2p, but not Yrb1p, and yrb2 cells were found to have a defect in nuclear export signal (NES)-dependent nuclear protein export. From these results together, the ability of Xpol/Crmlp to export NES-proteins is suggested to be enhanced by both Yrb2p and Gsplp, and thereby disruption of YRB2 retards nuclear protein export, resulting in the mitotic delay.
1This work was supported by Granta-in-Aid for Specially Promoted Research from the Ministry of Education, Science, Sports and Culture of Japan, and by a grant from the HFSP.
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