| Project/Area Number |
25860256
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Human genetics
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| Research Institution | Fujita Health University |
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Principal Investigator |
KATO Takema 藤田保健衛生大学, 総合医科学研究所, 助教 (20387690)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | PATRR / 染色体転座 / パリンドローム / t(3;8)(p14;q24) / FRA3B / 染色体脆弱部位 |
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| Outline of Final Research Achievements |
In this study, we identified novel palindrome-mediated translocations with the t(3;8)(p14;q24) and t(8;22)(q24;q11). Detailed sequence analysis of both junction breakpoints have been resolved by next generation sequencing. To predict the mechanism of translocation generation, derivative sequences were aligned to entire palindrome sequences. The translocation junction is often accompanied by symmetric deletions at the center of both palindrome sequences. Rejoining occurs with minimal homology between the translocation partners. Remarkably, comparison of both derivative sequences shows identical breakpoint junctions between them, which likely represent products of two independent events on the basis of a classical model. Our data suggest the hypothesis that interactions between the two PATRRs prior to the translocation event might trigger illegitimate recombination resulting in the recurrent palindrome-mediated translocation.
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