| Project/Area Number |
13680782
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
SONODA Eiichiro Kyoto University, Faculty of Medicine, Dept. of Radiation Genetics, associate professor, 医学研究科, 助教授 (50281093)
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| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2001: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | Sister Chromatid Cohesion / Rad21 / Kinetochore function / Chromosomal instability / DT40 / Cohesin / IN CENP |
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| Research Abstract |
Proteolytic cleavage of the cohesin subunit Rad21/Scc1 is a consistent feature of anaphase onset, although temporal differences exist between eukaryotes in cohesin loss from chromosome arms, as distinct from centromeres. We examined the effects of genetic deletion of Rad21/Scc1in chicken DT40 cells by using tet-repressive conditional system. We found that vertebrate Scc1 is an essential protein and is required for sister chromatid cohesion in interphase and mitosis, but not for chromosome condensation. Loss of sister chromatid cohesion also impedes the homologous recombinational repair of DNA damage. Chromosome misalignment at metaphase results in a miitotic arrest or delay in Scc1deficient cells, with aberrant disjunction at anaphase-potentially implicating *ohesion defects in aneuploidy. Surprisingly, we also found that Scc1 deficiency disrupts the centromere localization of the chromosome passenger, INCENP. These findings suggest additional roles for Scc1 at centromeres, in the control of kinetochore function per se
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