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MBC in Press, published online ahead of print August 18, 2004
Mol. Biol. Cell 10.1091/mbc.E04-01-0067

A more recent version of this article appeared on November 1, 2004
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Submitted on January 28, 2004
Revised on July 22, 2004
Accepted on August 3, 2004

S. pombe RanGAP Homolog, SpRna1, Is Required for Centromeric Silencing and Chromosome Segregation

Ayumi Kusano,* Tomoko Yoshioka, Hitoshi Nishijima, Hideo Nishitani, and Takeharu Nishimoto{dagger}

Department of Molecular Biology, Graduate School of Medical Science, Kyushu University, Higashi-ku, Fukuoka 812-8582, Japan

Monitoring Editor: Tony Hunter

We isolated eleven independent temperature-sensitive (ts) mutants of S. pombe RanGAP, SpRna1 that have several amino-acid changes in the conserved domains of RanGAP. Resulting Sprna1ts showed a strong defect in mitotic chromosome segregation, but did not in nucleocytoplasmic transport and microtubule formation. In addition to Sprna1+ and Spksp1+, the clr4+ (histone H3-K9 methyltransferase), the S. pombe gene, SPAC25A8.01c, designated snf2SR+ (a member of the chromatin remodeling factors, Snf2 family with DNA-dependent ATPase activity), but not the spi1+ (S. pombe Ran homolog), rescued a lethality of Sprna1ts. Both Clr4 and Snf2 were reported to be involved in heterochromatin formation essential for building the centromeres. Consistently, Sprna1ts was defective in gene-silencing at the centromeres. But a silencing at the telomere, another heterochromatic region, was normal in all of Sprna1ts strains, indicating SpRna1 in general did not function for a heterochromatin formation. snf2SR+ rescued a centromeric silencing defect and {Delta}clr4+ was synthetic lethal with Sprna1ts. Taken together, SpRna1 was suggested to function for constructing the centromeres, by cooperating with Clr4 and Snf2SR. Loss of SpRna1 activity, therefore, caused chromosome missegregation.

*Present address: Research Organization of Information and Systems, National Institute of Genetics, Genetics Strains Research Center, Laboratory for Frontier Research, 1111 Yata Mishima, 411-8540, Japan.

{dagger}Corresponding author. E-mail: tnishi{at}mailserver.med.kyushu-u.ac.jp






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