| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Research Abstract |
Mito-mice (mitochondrial disease model mice) have a characteristic inheritance pattern of deleted mitochondrial DNA (ΔmtDNA). When mother mito-mice are young, their offspring have high ΔmtDNA, but when mother mito-mice get older, their offspring have lower ΔmtDNA than their elder siblings. This study hypothesized that this phenomenon is governed by intra-cellular scavenging organelle, autophagosome, and examined how ΔmtDNA changes if mother mito-mice don't have functional autophgosomes. In this study, Atg7 KO mice were used as autophagosome deleted mice. Since homogenous Atg7 KO mice die immediate after birth, ovaries of obtained Atg7 deleted mito-mice with ΔmtDNA were transplanted into healthy mice, and time-dependent change of ΔmtDNA amount in oocytes was examined. In the homogeneous Atg7 KO mice, the decrease of ΔmtDNA were milder than those of wild-type and heterogenous Atg7 KO mice. This result implies that ΔmtDNA decrease in oocytes with mother's aging might be controlled by intra-cellular autophagosomes. However, the number of experiments repeated was not enough, and further repetitions will be required to confirm the result.
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