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Matsuo, Yoichiro*; Izumi, Yoshinobu*; Hase, Yoshihiro; Sakamoto, Ayako; Shimizu, Kikuo*
JAEA-Review 2014-050, JAEA Takasaki Annual Report 2013, P. 119, 2015/03
no abstracts in English
Shimizu, Kikuo*; Matsuo, Yoichiro*; Izumi, Yoshinobu*; Hase, Yoshihiro; Nozawa, Shigeki; Sakamoto, Ayako; Narumi, Issei
JAEA-Review 2010-065, JAEA Takasaki Annual Report 2009, P. 79, 2011/01
Matsuo, Yoichiro*; Nishijima, Shigehiro*; Hase, Yoshihiro; Nozawa, Shigeki; Sakamoto, Ayako; Narumi, Issei; Shimizu, Kikuo*
JAEA-Review 2009-041, JAEA Takasaki Annual Report 2008, P. 75, 2009/12
no abstracts in English
Matsuo, Yoichiro*; Nishijima, Shigehiro*; Hase, Yoshihiro; Sakamoto, Ayako; Narumi, Issei; Shimizu, Kikuo*
JAEA-Review 2008-055, JAEA Takasaki Annual Report 2007, P. 60, 2008/11
no abstracts in English
Matsuo, Yoichiro*; Nishijima, Shigehiro*; Hase, Yoshihiro; Sakamoto, Ayako; Yokota, Yuichiro; Narumi, Issei; Shimizu, Kikuo*
JAEA-Review 2007-060, JAEA Takasaki Annual Report 2006, P. 86, 2008/03
no abstracts in English
Takahashi, Shinya*; Sakamoto, Ayako; Tanaka, Atsushi; Shimizu, Kikuo*
Plant Physiology, 145(3), p.1052 - 1060, 2007/11
Times Cited Count:15 Percentile:37.85(Plant Sciences)To clarify the functions of AtREV1 protein, we expressed it in E. coli and purified it. The deoxynucleotidyl transferase activity of the recombinant AtREV1 was examined in a primer extension assay . The recombinant AtREV1 transferred one or two nucleotides to the primer end. Especially, it efficiently inserted dCMP regardless of the opposite base. AtREV1 also inserted a dCMP opposite the apurinic/apyrimidinic (AP) sites, which are physiologically generated or induced by various DNA-damaging agents. However, AtREV1 had no insertion activities against UV-inducible DNA lesions. Although the substrate specificity of AtREV1 was rather narrow in the presence of magnesium ion, it widened in the presence of manganese ion. These results suggest that AtREV1 serves as a deoxycytidyl transferase in plant cells.
Matsuo, Yuichiro*; Nishijima, Shigehiro*; Hase, Yoshihiro; Sakamoto, Ayako; Tanaka, Atsushi; Shimizu, Kikuo*
Mutation Research; Fundamental and Molecular Mechanisms of Mutagenesis, 602(1-2), p.7 - 13, 2006/12
Times Cited Count:28 Percentile:58.33(Biotechnology & Applied Microbiology)no abstracts in English
Matsuo, Yoichiro*; Nishijima, Shigehiro*; Hase, Yoshihiro; Sakamoto, Ayako; Tanaka, Atsushi; Shimizu, Kikuo*
no journal, ,
no abstracts in English
Matsuo, Yoichiro*; Nishijima, Shigehiro*; Hase, Yoshihiro; Sakamoto, Ayako; Tanaka, Atsushi; Shimizu, Kikuo*
no journal, ,
no abstracts in English
Matsuo, Yoichiro*; Nishijima, Shigehiro*; Shimizu, Kikuo*; Hase, Yoshihiro; Sakamoto, Ayako; Narumi, Issei
no journal, ,
no abstracts in English
Matsuo, Yoichiro*; Nishijima, Shigehiro*; Hase, Yoshihiro; Sakamoto, Ayako; Narumi, Issei; Shimizu, Kikuo*
no journal, ,
no abstracts in English
Sakamoto, Ayako; Takahashi, Shinya*; Nakagawa, Mayu; Tanaka, Atsushi; Shimizu, Kikuo*; Narumi, Issei
no journal, ,
The harmful effects of UVB in the sunlight are unavoidable problems for higher plants that live on photosynthesis. To keep the genomic information intact, plant cells remove the UV damage formed on the DNA by photoreactivation. Plants also have dark-repair and damage tolerance pathways to prevent growth defect caused by DNA damage. Here we report about and genes, which encode specific polymerases to bypass DNA damage. The - or -disrupted plants were more sensitive to UVB, -ray, and DNA crosslink agents than the wild type, suggesting that these REV proteins are required for plant damage tolerance. Although bacterially expressed AtREV1 protein inserted a dCMP at opposite the AP site, it failed to bypass two major UV damages . This inconsistency makes us propose a novel function of AtREV1 in the UV-tolerance pathway. To evaluate the function of AtREV3 and AtREV1 in bypassing UV-damage, we have detected replication errors that often emerged during damage bypass process. The point-mutated, non-functional genes were introduced into Arabidopsis plants and reversion events (mutations) were detected by blue GUS+ sectors on the somatic tissues. We found that a disruption of or reduced the mutation frequency to 1/4 of the level of the wild type. These results suggest that the AtREV3 and AtREV1 are bypassing the DNA damage in error-prone manner.
Sakamoto, Ayako; Takahashi, Shinya*; Iwai, Shigenori*; Shimizu, Kikuo*
no journal, ,
no abstracts in English
Matsuo, Yoichiro*; Nishijima, Shigehiro*; Hase, Yoshihiro; Yokota, Yuichiro; Sakamoto, Ayako; Narumi, Issei; Shimizu, Kikuo*
no journal, ,
no abstracts in English
Sakamoto, Ayako; Nakagawa, Mayu; Takahashi, Shinya*; Shimizu, Kikuo*; Tanaka, Atsushi; Narumi, Issei
no journal, ,
Matsuo, Yoichiro*; Nishijima, Shigehiro*; Hase, Yoshihiro; Sakamoto, Ayako; Narumi, Issei; Shimizu, Kikuo*
no journal, ,
no abstracts in English
Matsuo, Yoichiro*; Nishijima, Shigehiro*; Sakamoto, Ayako; Shimizu, Kikuo*
no journal, ,
no abstracts in English
Shimizu, Kikuo*; Matsuo, Yoichiro*; Izumi, Yoshinobu*; Nishijima, Shigehiro*; Hase, Yoshihiro; Sakamoto, Ayako; Narumi, Issei
no journal, ,
no abstracts in English
Izumi, Yoshinobu*; Matsuo, Yoichiro*; Sakamoto, Ayako; Takagi, Keiichi*; Hatashita, Masanori*; Kojima, Takao*; Shimizu, Kikuo*
no journal, ,
In cases of ion-beam irradiations, several features of deep interest can be observed, contrasting with the low-LET radiations such as -rays. In order to elucidate the induction mechanisms of mutations peculiar to ion beams, carbon-ion beams with LETs of 13 keV/m - 107 keV/m and proton beam with LET of 0.45 keV/m were irradiated to budding yeast. Carbon-ion beams and proton beam irradiation were performed in TIARA or HIMAC, and WERC, respectively. After irradiations, survival ratios and mutation frequencies were analyzed as well as sequencing and gene expression analyses. In order to elucidate the molecular mechanisms of mutagenesis caused by radiations, we used (BER-) which is deficient in the elimination of 8-oxodGTP and (MMR-) deficient in the mismatch-repair function. For comparison, we also used (NHEJ-) and (HR-) that were deficient in the double-strand breaks (DSBs)-repair function.
Matsuo, Yoichiro*; Izumi, Yoshinobu*; Hase, Yoshihiro; Nozawa, Shigeki; Sakamoto, Ayako; Narumi, Issei; Shimizu, Kikuo*
no journal, ,
no abstracts in English