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Article
Nature 442, 45-50 (6 July 2006) | doi:10.1038/nature04881; Received 26 January 2006; Accepted 5 May 2006
Selective elimination of messenger RNA prevents an incidence of untimely meiosis
Yuriko Harigaya1, Hirotsugu Tanaka1,4, Soichiro Yamanaka1, Kayoko Tanaka1, Yoshinori Watanabe1,4, Chihiro Tsutsumi3, Yuji Chikashige3, Yasushi Hiraoka3, Akira Yamashita2 & Masayuki Yamamoto1,2
- Department of Biophysics and Biochemistry, Graduate School of Science, and
- Molecular Genetics Research Laboratory, University of Tokyo, Hongo, Tokyo 113-0033, Japan
- Kansai Advanced Research Center, National Institute of Information and Communications Technology, Kobe 651-2492, Japan
- †Present addresses: Toukoudai Research Center, Astellas Pharma Inc., Toukoudai, Tsukuba 300-2698, Japan (H.T.); Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan (Y.W.)
Correspondence to: Masayuki Yamamoto1,2 Correspondence and requests for materials should be addressed to M.Y. (Email: yamamoto@biochem.s.u-tokyo.ac.jp). The entire microarray data obtained in this study has been deposited in the Gene Expression Omnibus (GEO), under the accession number GSE3314.
Abstract
Much remains unknown about the molecular regulation of meiosis. Here we show that meiosis-specific transcripts are selectively removed if expressed during vegetative growth in fission yeast. These messenger RNAs contain a cis-acting region—which we call the DSR—that confers this removal via binding to a YTH-family protein Mmi1. Loss of Mmi1 function severely impairs cell growth owing to the untimely expression of meiotic transcripts. Microarray analysis reveals that at least a dozen such meiosis-specific transcripts are eliminated by the DSR–Mmi1 system. Mmi1 remains in the form of multiple nuclear foci during vegetative growth. At meiotic prophase these foci precipitate to a single focus, which coincides with the dot formed by the master meiosis-regulator Mei2. A meiotic arrest due to the loss of the Mei2 dot is released by a reduction in Mmi1 activity. We propose that Mei2 turns off the DSR–Mmi1 system by sequestering Mmi1 to the dot and thereby secures stable expression of meiosis-specific transcripts.
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