| Budget Amount *help |
¥122,330,000 (Direct Cost: ¥94,100,000、Indirect Cost: ¥28,230,000)
Fiscal Year 2015: ¥23,140,000 (Direct Cost: ¥17,800,000、Indirect Cost: ¥5,340,000)
Fiscal Year 2014: ¥23,140,000 (Direct Cost: ¥17,800,000、Indirect Cost: ¥5,340,000)
Fiscal Year 2013: ¥24,440,000 (Direct Cost: ¥18,800,000、Indirect Cost: ¥5,640,000)
Fiscal Year 2012: ¥24,180,000 (Direct Cost: ¥18,600,000、Indirect Cost: ¥5,580,000)
Fiscal Year 2011: ¥27,430,000 (Direct Cost: ¥21,100,000、Indirect Cost: ¥6,330,000)
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| Outline of Final Research Achievements |
It has been known that there are chromosomal fragile sites such as common fragile sites (CFS) among non-coding DNA regions that are prone to break upon replication stress and are conserved throughout evolution. Therefore these fragile sites are supposed to have a critical function for sustaining life, but its exact role remains unknown. In this study, we focused on chromatin dynamics at the fragile sites and the mechanisms of checkpoint signaling that stabilizes stalled replication forks. In particular, we analyzed (1) genome wide distribution of a key Fanconi anemia factor FANCD2 upon replication stress, (2) mechanisms of fork stabilization and breakage by proteomics analysis, (3) activation mechanisms of ATR-ATRIP replication checkpoint kinase.
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