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Published March 12, 2002 | Published
Journal Article Open

Multiple telophase arrest bypassed (tab) mutants alleviate the essential requirement for Cdc15 in exit from mitosis in S. cerevisiae


Background: The Mitotic Exit Network (MEN) proteins – including the protein kinase Cdc15 and the protein phosphatase Cdc14 – are essential for exit from mitosis in Saccharomyces cerevisiae. To identify downstream targets of the MEN, we sought telophase arrest bypassed (tab) mutations that bypassed the essential requirement for CDC15. Previous studies identified net1^(tab2-1) and CDC14^(TAB6-1) as mutations in the RENT complex subunits Net1 and Cdc14, respectively, and revealed that the MEN acts by promoting release of Cdc14 from its nucleolar Net1 anchor during anaphase. However, the remaining tab mutants were not characterized. Results: Fourteen out of fifteen tab mutants were mapped to three recessive (tab1-tab3) and three dominant (TAB5-TAB7) linkage groups. We show that net1^(tab2-1) enables growth of tem1Δ, cdc15Δ, dbf2Δ dbf20Δ, and mob1Δ, but not cdc5Δ or cdc14Δ, arguing that whereas the essential task of the first four genes is to promote exit from mitosis, CDC5 possesses additional essential function(s). net1^(tab2-1) but not CDC14^(TAB6-1) resulted in a high rate of chromosome loss, indicating that Net1 promotes accurate chromosome segregation in addition to its multiple known roles. Finally, TAB1 was shown to be MTR10, a gene encoding nuclear transport receptor/adaptor. In some of the tab mutants including mtr10^(tab1-1), defective nuclear export of the ribosomal protein Rpl11b was observed. Furthermore, the transport-defective -31 allele of the karyopherin SRP1, but not the transport competent -49 allele, exhibited a tab phenotype. Conclusions: Transport-defective mutations in two karyopherins can bypass cdc15Δ, suggesting that the function of the MEN is to promote mitotic exit by regulating nuclear transport.

Additional Information

© Shou and Deshaies. 2002. This article is published under license to BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL. Received: 11 December 2001. Accepted: 12 March 2002. Published: 12 March 2002. Special thanks go to Ramzi Azzam for mapping the putative "tab4" mutation to the tab1 linkage group (Table 2) and Kathleen Sakamoto for performing the Nop1 immunofluorescence experiment (Table 2). We thank R. Azzam, K. Sakamoto, M. Budd, R. Feldman, B. Hay, P. Sternberg, and R. Verma for discussions; H. Mountain, P. Philippsen, A. Varshavsky, B. Futcher, and P. Silver for pMET3, S. pombe his5 +, UPL, HA3, and RPL11B-GFP plasmids, respectively; F. Uhlmann and H. Rao for the SUP11/URA3 sectoring strain; M. Nomura, L. Johnston, and F. Luca for srp1, dbf2Δdbf20Δ [pRS316-DBF2], and mob1Δ [pRS316-MOB1] strains, respectively; C. Thompson for yeast genomic library, and D. Kellogg, R. Feldman, and J. Aris for anti-Clb2, anti-Sic1, and anti-Nop1, respectively. W.S. was a Howard Hughes Medical Institute predoctoral fellow.

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