@article{oai:repo.qst.go.jp:00047245,
 author = {Sugaya, Kimihiko and Ishihara, Yoshie and Sugaya, Keiko and Inoue, Sonoe and 菅谷 公彦 and 石原 よし江 and 菅谷 恵子 and 井上 園江},
 issue = {1},
 journal = {American Journal of Molecular Biology},
 month = {Jan},
 note = {A temperature-sensitive (ts) mutant of the CHO-K1 cell line, tsTM18, grows at 34C but not at 39C. Smu1 is the gene responsible for the ts defect of tsTM18 cells. We found that the Smu1 ts defect appeared to alter the localization (as indicated by enlargement of speckles) of SRSF1 (SF2/ASF) in tsTM18 cells cultured at 39C, suggesting a functional association between Smu1 and SRSF1. Speckles are subnuclear structures that may function as storage/assembly/modification compartments to supply splicing factors to active transcription sites. In the present study, we found that the ts defect of Smu1 affected the nuclear localization of a splicing factor, SRSF2 (SC35), and factors involved in the exon-exon junction complex, Y14 and ALY. Reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that the ts defect of Smu1 affected alternative splicing of endogenous Clk1/Sty and SRSF2 genes. Mammalian Clk family kinases are shown to phosphorylate serine/arginine (SR) proteins in vitro and SRSF1 in vivo. RT-PCR analysis of Clk1/Sty showed an accumulation of the truncated form lacking kinase activity in tsTM18 cells incubated at 39C. These data indicate that an accumulation of kinase-negative Clk1/Sty may lead to alteration of the localization of factors related to splicing resulting in the enlargement of speckles.},
 pages = {38--44},
 title = {Characterization of the role of Smu1 in nuclear localization of splicing factors in the mammalian temperature-sensitive mutant},
 volume = {3},
 year = {2013}
}