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First published online May 4, 2004
doi: 10.1242/10.1242/jcs.01078

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Suppression of a mitotic mutant by tRNA-Ala anticodon mutations that produce a dominant defect in late mitosis

Department of Gene Mechanisms, Graduate School of Biostudies, Kyoto University. Kitashirakawa-Oiwakecho, Sakyo-ku, Kyoto 606-8501, Japan

^* Author for correspondence (e-mail: yanagida{at}kozo.biophys.kyoto-u.ac.jp)

Accepted 5 January 2004

Cold-sensitive dominant mutants scn1 and scn2 of Schizosaccharomyces pombe were isolated by their ability to suppress temperature-sensitive cut9-665 defective in an essential subunit (human Apc6/budding yeast Cdc16 ortholog) of anaphase promoting complex/cyclosome (APC/C). APC/C mutants were defective in metaphase/anaphase transition, whereas single scn mutants showed the delay in anaphase spindle elongation at 20°C. The scn mutants lost viability because of chromosome missegregation, and were sensitive to a tubulin poison. To understand the scn phenotypes, mutant genes were identified. Surprisingly, scn1 and scn2 have the same substitution in the anticodon of two different tRNA-Ala (UGC) genes. UGC was altered to UGU so that the binding of the tRNA-Ala to the ACA Thr codon in mRNA became possible. As cut9-665 contained an Ala535Thr substitution, wild-type Cut9 protein was probably produced in scn mutants. Indeed, plasmid carrying tRNA-Ala (UGU) conferred cold-sensitivity to wild-type and suppressed cut9-665 in a dominant fashion. The previously identified scn1⁺ (renamed as scn3⁺) turned out to be a high copy suppressor for scn1 and scn2. These are the first tRNA mutants that cause a mitotic defect.

Key words: Mitosis, Anaphase, tRNA mutant, Anticodon, Dominant mutation

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