|Mizuki Ohno||Last modified date：2021.09.14|
Assistant Professor / Department of Medical Biophysics & Radiation Biology, / Department of Basic Medicine / Faculty of Medical Sciences
|Mizuki Ohno||Last modified date：2021.09.14|
|1.||Mizuki OHNO, Kunihiko SAKUMI, Noriko TAKANO,Kosuke TESHIMA, Kyoko HIDAKA, Yoshimichi NAKATSU, Teruhisa TSUZUKI
, Detection of de novo germline mutations in DNA repair-deficient mice lines
, The Joint Meeting of The 6th Asian Congress on Environmental Mutagens(ACEM) and the 48th Annual Meeting of the Japanese Environmental Mutagen Society(JEMS), 2019.11.
|2.||Mizuki Ohno, Kunihoko Sakumi, Noriko Takano, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Toward understanding de novo germline mutations in mammals, 日本放射線影響学会第62回大会, 2019.11.|
|3.||Teruhisa Tsuzuki, Mizuki Ohno, Noriko Takano, Kenichi Taguchi, Yoshimichi Nakatsu, Oxidative stress-induced tumorigenesis: Lesson from the experiments with DNA repair-deficient mice., Beijing Symposium on “Genomic Stability and Accurate Gene Expression under Oxidative Stress”, 2018.11.|
|4.||Mizuki Ohno, Noriko Takano, Kunihiko Sakumi, Teruhisa Tsuzuki, The impact of DNA repair status on germline mutation rate and spectra in mice, SMBE2018 (Society for Molecular Biology and Evolution), 2018.07.|
|5.||Yoshimichi Nakatsu, Noriko Takano, Mizuki Ohno, Satoshi Kitazaki, Kazunori Koga, Akiyo Tanaka, Masaharu Shiratani, Application of transgenic mice to analyze genotoxic effects induced by non-thermal atmospheric air plasma, 10th Anniversary International Symposium on Advanced Plasma Science and its Applications for Nitrides and Nanomaterials/11th International Conference on Plasma-Nano Technology & Science. (ISPlasma2018 / IC-PLANTS2018), 2018.03.|
|6.||Teruhisa Tsuzuki, Mizuki Ohno, Noriko Takano, Kenichi Taguchi, Yusaku Nakabeppu, Yoshimichi Nakatsu, Oxidative stress-induced tumorigenesis: Lesson from the experiments with DNA repair-deficient mice, The 14th Transgenic Technology Meeting, 2017.10.|
|7.||Teruhisa Tsuzuki, Mizuki Ohno, Noriko Takano, Ken-ichi Taguchi, Yusaku Nakabeppu, Yoshimichi Nakatsu, Oxidative stress-induced tumorigenesis: Lesson from the experiments with
DNA repair-deficient mice, The 14th Transgenic Technology Meeting, 2017.10.
|8.||Mizuki Ohno, Noriko Takano, Kyouko Hidaka, Kunihiko Sakumi, Yusaku Nakabeppu, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Somatic mutation analysis of oxidative stress-induced colon cancer model
大腸癌モデルマウスを用いた酸化ストレス誘発発がんと体細胞突然変異の解析, 第76回日本癌学会学術総会, 2017.09, Colorectal cancer (CRC) is one of the most common cancers, and oxidative stress is predicted to play an important role in the pathogenesis of CRC. MUTYH is an adenine DNA glycosylase that suppresses oxidative stress-induced mutagenesis by removing adenine mispaired with 8-oxoguanine (8-oxoG), a major oxidative DNA damage. Biallelic mutations in MUTYH gene cause an inherited predisposition to CRC, known as MUTYH-associated polyposis (MAP). Since oxidative stress-induced mutations would be relevant to driving force for tumorigenesis, we studied the property of somatic mutations in the intestines of Mutyh-deficient mice. We found a clear correlation among the levels of oxidative stress, the induced mutation frequency in pre-cancerous tissues, and the tumor incidence. Moreover, whole-exome analysis of tumors developed in the mice revealed a specific mutational pattern; predominant G:C > T:A mutations in the specific sequence contexts, which is resulted from unrepaired 8-oxoG:A mispairings. This pattern was also observed in the somatic mutations detected in the tumors from MAP patients. Thus, avoiding excess oxidative stress can be helpful to reduce a lifetime risk of CRC for MAP patients..
|9.||Yoshimichi Nakatsu, Noriko Takano, Mizuki Ohno, S. Kitazaki, K. Koga, A. Tanaka, M. Shiratani, T. Tsuzuki, Analyses of Oxidative Mutagenesis and Carcinogenesis Using Genetically Modified Mice: Application to Plasma Medicine, 4th International Workshop on Plasma for Cancer Treatment(IWPCT2017), 2017.03.|
|10.||大野 みずき, 作見 邦彦, 中別府 雄作, Regulation of base substitution mutagenesis and chromosome recombination induced by 8-oxoguanine accumulated in the genome, 日本分子生物学会, 2016.12.|
|11.||Mizuki Ohno, Noriko Takano, Kunihiko Sakumi, Ryutaro Fukumura, Yuki Iwasaki, Toshimichi Ikemura, Yoichi Gondo, Yusaku Nakabeppu, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Role of the oxidative DNA damage repair system in somatic and germline mutations in mice, Zing conference "Genome Integrity", 2015.08.|
|12.||Ohno Mizuki, Takano Noriko, SAKUMI Kunihiko, Ryutaro Fukumura, Yuki Iwasaki, Toshimichi Ikemura, Yoichi Gondo, Yusaku Nakabeppu, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Influence of oxidative DNA damage on the rate of somatic and germline mutation, 15th International Congress of Radiation Research, 2015.05.|
|13.||Mizuki Ohno, Oxidative DNA damage and its repair system: implications for de novo germline mutations , 第38回日本分子生物学会, 2014.11.|
|14.||大野 みずき, 鷹野典子, 中津 可道, 中別府 雄作, 續 輝久, Oxidative stress-induced tumorigenesis in the small intestine of Mutyh-deficient mouse, 第73回日本癌学会学術総会, 2014.09.|
|15.||Yusaku Nakabeppu, Ohno Mizuki, SAKUMI Kunihiko, Oxidation of nucleic acids and control mechanisms of genetic diversity in mammals, International Symposium on Germline Mutagenesis and Biodiversification, 2014.03.|
|16.||Ohno Mizuki, SAKUMI Kunihiko, FUKUMURA Ryutaro, IWASAKI Yuki, IKEMURA Toshimichi, Teruhisa Tsuzuki, GONDO Yoichi, Yusaku Nakabeppu, 8-Oxoguanine causes spontaneous de novo germline mutations : a study from the mutator mouse line, SMBE Satellite Meeting / NIG International Symposium: The Causes of Genome Evolution, 2014.03.|
|17.||Yusaku Nakabeppu, Ohno Mizuki, SAKUMI Kunihiko, Oxidation of nucleic acids by reactive oxygen species and control mechanisms of genetic diversity in mammals, International Symposium between Kyushu University Post-Global Centers of Excellence Program and School of Biomedical Sciences, 2014.02.|
|18.||8-Oxoguanine repair system contribute to maintain stable phenotype of inbred mouse strain .|
|19.||Deficiency of 8-oxoguanine repair mechanisms increases spontaneous mutation frequency in mouse germ line and consequently causes hereditary congenital abnormalities.|
|20.||A study of radiation-induced oxidative DNA damage and its repair in mouse intestine.|
|21.||Analysis of radiation induced DNA damage and its repair in intestine and testis.|
|22.||8-oxoguanine increases the frequency of meiotic homologous recombination via DNA strand breaks.|
|23.||It is well known that reactive oxygen species are generated not only by environmental factors but also by normal cellular metabolisms. We have been focusing on the effect of oxidative DNA damage to genome integrity. Previously we suggested that 8-oxoguanine (8-oxoG) is one of the main causes of base substitution and homologous recombination in the mammalian genome. To elucidate the influence of 8-oxoG on germ-line mutations, we analyzed DNA damage, damage response and resulting homologous recombination using testes derived from Ogg1, Mth1 deficient mice or X-ray irradiated wild-type mice. An increased amount of DNA damage as well as an activation of damage response was observed in the spermatocytes derived from testis of these mice. Moreover, we found an increased frequency of meiotic homologous recombination in Ogg1 or Mth1 deficient mice. .|
|24.||Biological sensitivity to radiation differs among cell and organ types, as well as their state of cell cycle when irradiated. This difference in radiation sensitivity can be attributed to multiple factors, including the amount or kind of DNA damage and mechanisms of damage response and repair.
The effect of DNA exposure to radiation is both direct and indirect. The direct effect is the physical break, single or double, in DNA following ionizing radiation exposure. Free radical species, a product of the interaction between radiation and cellular water, results in many chemical and biological changes, producing an indirect effect. Of the latter, prolonged oxidative stress caused by low LET radiation is a risk factor for the alteration of genetic information. Mutations in somatic cells can result in cancer and other diseases, while those occurred in germ cells could potentially be inherited to offspring, and lead to congenital disorders.
To study the effects of radiation-induced oxidative DNA damage and its repair mechanism, we analyzed the DNA damage response in the testis and intestine of X-ray irradiated mice, including damage status, degree of cell death and cell proliferation. Radiation exposure for 2 days and 7 days at 0.5, 1, 2, and 4Gy revealed a pattern of increased immunoreactivity in gH2AX, 53BP1 and Rad51, as well as a decrease in the number of BrdU positive cells within the testis. The same result was not observed in intestinal samples at those time points. The nuclear content of 8-oxoguanine, an oxidized form of guanine, was also analyzed together with the expression of repair factors in different cell types.
|25.||Production and analysis of the Ogg1, Mth1, Mutyh triple knockout mouse strain.|
|26.||The influence of oxidative damaged base on germ-line mutation.|