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Nature 442, 45-50 (6 July 2006) | doi:10.1038/nature04881; Received 26 January 2006; Accepted 5 May 2006

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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

  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. Kansai Advanced Research Center, National Institute of Information and Communications Technology, Kobe 651-2492, Japan
  4. †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.

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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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