2009 Fiscal Year Final Research Report
Crosstalk between cell cycle regulatory mechanism and DNA repair
| Project/Area Number |
19681004
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Kobe University |
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Principal Investigator |
NISHI Ryotaro Kobe University, 自然科学系先端融合研究環・バイオシグナル研究センター, 助教 (80446525)
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| Project Period (FY) |
2007 – 2009
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| Keywords | 放射線生物影響 / DNA修復 / 細胞周期 |
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| Research Abstract |
Nucleotide excision repair (NER) is a versatile DNA repair mechanism that eliminates a wide variety of DNA lesions including UV-induced thymine dimers. XPC complex plays an essential role in DNA damage recognition of NER. Although centrin 2 which belongs to calmodulin super family was suggested to enhance NER by increasing DNA-binding activity of XPC, the precise mechanism of this enhancement remains to be elucidated. Biochemical studies using truncated mutant of centrin 2 indicated that C-terminal domain of centrin 2 is sufficient for enhancement of reconstituted NER and DNA-binding activity of XPC via complex formation with XPC. On the contrary, N-terminal domain interacted with UV-DDB, which is a component of E3 ligase ubiquitylating XPC according to UV irradiation. Electrophoretic mobility shift assay suggested that centrin 2 aids in formation of complex between XPC and UV-DDB on damaged-DNA. Furthermore, UV-C induced ubiquitylation of XPC was compromised in the absence of centrin 2, implying that centrin 2 might regulate ubiquitylation of XPC by interacting with two damage recognition factors via structurally independent two domains.
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Research Products
(6 results)
