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Eukaryotic Cell, August 2006, p. 1301-1313, Vol. 5, No. 8
1535-9778/06/$08.00+0     doi:10.1128/EC.00099-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Spo5/Mug12, a Putative Meiosis-Specific RNA-Binding Protein, Is Essential for Meiotic Progression and Forms Mei2 Dot-Like Nuclear Foci{dagger}

Takashi Kasama,1,{ddagger} Akira Shigehisa,1,{ddagger} Aiko Hirata,2 Takamune T. Saito,1 Takahiro Tougan,1 Daisuke Okuzaki,1 and Hiroshi Nojima1*

Department of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan,1 Departments of Integrated Biosciences, Graduate School of Frontier Sciences, University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa, Chiba 277-8562, Japan2

Received 7 April 2006/ Accepted 12 May 2006

We report here a functional analysis of spo5+(mug12+) of Schizosaccharomyces pombe, which encodes a putative RNA-binding protein. The disruption of spo5+ caused abnormal sporulation, generating inviable spores due to failed forespore membrane formation and the absence of a spore wall, as determined by electron microscopy. Spo5 regulates the progression of meiosis I because spo5 mutant cells display normal premeiotic DNA synthesis and the timely initiation of meiosis I but they show a delay in the peaking of cells with two nuclei, abnormal tyrosine 15 dephosphorylation of Cdc2, incomplete degradation of Cdc13, retarded formation and repair of double strand breaks, and a reduced frequency of intragenic recombination. Immunostaining showed that Spo5-green fluorescent protein (GFP) appeared in the cytoplasm at the horsetail phase, peaked around the metaphase I to anaphase I transition, and suddenly disappeared after anaphase II. Images of Spo5-GFP in living cells revealed that Spo5 forms a dot in the nucleus at prophase I that colocalized with the Mei2 dot. Unlike the Mei2 dot, however, the Spo5 dot was observed even in sme2{Delta} cells. Taken together, we conclude that Spo5 is a novel regulator of meiosis I and that it may function in the vicinity of the Mei2 dot.


* Corresponding author. Mailing address: Department of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan. Phone: 81 6 6875 3980. Fax: 81 6 6875 5192. E-mail: snj-0212{at}biken.osaka-u.ac.jp.

{dagger} Supplemental material for this article may be found at http://ec.asm.org/.

{ddagger} These authors contributed equally to this work.


Eukaryotic Cell, August 2006, p. 1301-1313, Vol. 5, No. 8
1535-9778/06/$08.00+0     doi:10.1128/EC.00099-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




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