1. Department of Biophysics and Biochemistry, Graduate School of Science, and
2. Molecular Genetics Research Laboratory, University of Tokyo, Hongo, Tokyo 113-0033, Japan
3. Division of Cell Proliferation, National Institute for Basic Biology, Okazaki, Aichi 444-0867, Japan
4. Cell Cycle Control Group, Marie Curie Research Institute, The Chart, Oxted, Surrey RH8 0TL, UK
5. Present address: NIEHS, NIH, Research Triangle Park, North Carolina 27709-2233, USA

Correspondence to: Masayuki Yamamoto^1,2 Correspondence and requests for materials should be addressed to M.Y. (Email: myamamot@ims.u-tokyo.ac.jp).

Abstract

Meiosis is a special form of nuclear division to generate eggs, sperm and spores in eukaryotes. Meiosis consists of the first (MI) and the second (MII) meiotic divisions, which occur consecutively. MI is reductional, in which homologous chromosomes derived from parents segregate. MI is supported by an elaborate mechanism involving meiosis-specific cohesin and its protector¹. MII is equational, in which replicated sister-chromatids separate as in mitosis. MII is generally considered to mimic mitosis in mechanism. However, fission yeast Mes1p is essential for MII but dispensable for mitosis. The mes1-B44 mutant arrests before MII². Transcription of mes1 is low in vegetative cells and boosted in a narrow window between late MI and late MII³. The mes1 mRNA undergoes meiosis-specific splicing⁴. Here we show that Mes1p is a factor that suppresses the degradation of cyclin Cdc13p at anaphase I. Mes1p binds to Slp1p, an activator of APC/C (anaphase promoting complex/cyclosome), and counteracts its function to engage Cdc13p in proteolysis. Inhibition of APC/C-dependent degradation of Cdc13p by Mes1p was reproduced in a Xenopus egg extract. We therefore propose that Mes1p has a key function in saving a sufficient level of MPF (M-phase-promoting factor) activity required for the execution of MII.

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