小田　真由美 （オダ　マユミ）

Oda, Mayumi

写真a

所属（所属キャンパス）

医学部 医化学教室 （信濃町）

職名

専任講師（有期）

HP

外部リンク
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研究分野 【 表示 ／ 非表示 】

  • ライフサイエンス / 獣医学

  • ライフサイエンス / ゲノム生物学

  • ライフサイエンス / 循環器内科学

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研究テーマ 【 表示 ／ 非表示 】

  • エピゲノム, 

    2006年01月
    -
    継続中

    　研究概要を見る

    エピジェネティクス修飾とゲノム情報の関わりを中心に、発生・分化および疾患を考えていきたいと考えています。

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  • Genetic analysis of essential cardiac transcription factors in 256 patients with non-syndromic congenital heart defects

    Kodo Kazuki, Nishizawa Tsutomu, Furutani Michiko, Arai Shoichi, Ishihara Kazuaki, Oda Mayumi, Makino Shinji, Fukuda Keiichi, Takahashi Takao, Matsuoka Rumiko, Nakanishi Toshio, Yamagishi Hiroyuki

    Circulation Journal 76 （ 7 ） 1703 - 1711 2012年

    ISSN  1346-9843

    　概要を見る

    <p>Background: The genetic basis of most congenital heart defects (CHDs), especially non-syndromic and non-familial conditions, remains largely unknown. Methods and Results: DNA samples were collected from immortalized cell lines and original genomes of 256 nonsyndromic, non-familial patients with cardiac outflow tract (OFT) defects. Genes encoding NKX2.5, GATA4, GATA6, MEF2C, and ISL1, essential for heart development, were analyzed using PCR-based bidirectional sequencing. The transcriptional activity of proteins with identified sequence variations was analyzed using a luciferase assay. A novel sequence variant (A103V in MEF2C) was identified, in addition to 4 unreported non-synonymous sequence variants in 3 known causative genes (A6V in NKX2.5, T330R and S339R in GATA4, and E142K in GATA6) in 5 individuals. None of these was found in 500 controls without CHDs. In vitro functional assay showed that all proteins with identified sequence variations exhibited significant changes in transcriptional activity and/or synergistic activity with other transcription factors. Furthermore, overexpression of the A103V MEF2C variant in a fish system disturbed early cardiac development. Conclusions: New mutations in the transcription factors NKX2.5, GATA4, GATA6, and MEF2C that affect their protein function were identified in 2.3% (6/256) of patients with OFT defects. Our results provide the first demonstration of MEF2C mutation and suggest that disturbances in the regulatory circuits involving these cardiac transcription factors may cause a subset of non-syndromic and non-familial CHDs.</p>

  • Late-replicating heterochromatin is characterized by decreased cytosine methylation in the human genome

    Suzuki Masako, Oda Mayumi, Ramos María Paz, Pascual Marién, Lau Kevin, Stasiek Edyta, Agyiri Frederick, Thompson Reid F., Glass Jacob L., Jing Qiang, Sandstrom Richard, Fazzari Melissa J., Hansen R. Scott, Stamatoyannopoulos John A., McLellan Andrew S., Greally John M.

    Genome Research 21 （ 11 ） 1833 - 1840 2011年11月

    ISSN  1088-9051

    　概要を見る

    <p>Heterochromatin is believed to be associated with increased levels of cytosine methylation. With the recent availability of genome-wide, high-resolution molecular data reflecting chromatin organization and methylation, such relationships can be explored systematically. As well-defined surrogates for heterochromatin, we tested the relationship between DNA replication timing and DNase hypersensitivity with cytosine methylation in two human cell types, unexpectedly finding the later-replicating, more heterochromatic regions to be less methylated than early replicating regions. When we integrated gene-expression data into the study, we found that regions of increased gene expression were earlier replicating, as previously identified, and that transcription-targeted cytosine methylation in gene bodies contributes to the positive correlation with early replication. A self-organizing map (SOM) approach was able to identify genomic regions with early replication and increased methylation, but lacking annotated transcripts, loci missed in simple two variable analyses, possibly encoding unrecognized intergenic transcripts. We conclude that the relationship of cytosine methylation with heterochromatin is not simple and depends on whether the genomic context is tandemly repetitive sequences often found near centromeres, which are known to be heterochromatic and methylated, or the remaining majority of the genome, where cytosine methylation is targeted preferentially to the transcriptionally active, euchromatic compartment of the genome. © 2011 by Cold Spring Harbor Laboratory Press.</p>

  • Generation of induced pluripotent stem cells from human terminally differentiated circulating t cells

    Seki Tomohisa, Yuasa Shinsuke, Oda Mayumi, Egashira Toru, Yae Kojiro, Kusumoto Dai, Nakata Hikari, Tohyama Shugo, Hashimoto Hisayuki, Kodaira Masaki, Okada Yohei, Seimiya Hiroyuki, Fusaki Noemi, Hasegawa Mamoru, Fukuda Keiichi

    Cell Stem Cell 7 （ 1 ） 11 - 13 2010年07月

    ISSN  1934-5909

  • Trophoblast cell lineage in cloned mouse embryos

    Oda Mayumi, Shiota Kunio, Tanaka Satoshi

    Development Growth and Differentiation 52 （ 3 ） 285 - 291 2010年04月

    ISSN  0012-1592

    　概要を見る

    <p>Most conceptuses derived by somatic cell nuclear transfer (SCNT) in mice undergo developmental arrest as a result of embryonic or extraembryonic defects. Even when fetuses survive to term, prominent placental overgrowth or placentomegaly is often present, indicating that SCNT affects the development of trophoblast cell lineage. The trophoblast cell lineage is established at the blastocyst stage when the stem cell population of the trophoblast cell lineage resides in the polar trophectoderm. Therefore, it is possible that the developmental arrest and placentomegaly that accompany SCNT are induced by insufficient reprogramming of the donor somatic nucleus to enable the cells to acquire full potency as stem cells of the trophoblast cell lineage. Despite the abnormalities of the extraembryonic tissues of SCNT embryos, trophoblast stem (TS) cell lines have been successfully isolated from SCNT blastocysts and their properties appear to be indistinguishable from those of TS cells derived from native blastocysts. This suggests that SCNT does not affect the emergence and autonomous properties of TS cells. In this review, we discuss specification of cell lineage and the extent of reprogramming of TS cells in SCNT blastocysts. © 2010 Japanese Society of Developmental Biologists.</p>

  • Establishment of trophoblast stem cell lines from somatic cell nuclear-transferred embryos

    Oda Mayumi, Tanaka Satoshi, Yamazaki Yukiko, Ohta Hiroshi, Iwatani Misa, Suzuki Masako, Ohgane Jun, Hattori Naka, Yanagimachi Ryuzo, Wakayama Teruhiko, Shiota Kunio

    Proceedings of the National Academy of Sciences of the United States of America 106 （ 38 ） 16293 - 16297 2009年09月

    ISSN  0027-8424

    　概要を見る

    <p>Placental abnormalities occur frequently in cloned animals. Here, we attempted to isolate trophoblast stem (TS) cells from mouse blastocysts produced by somatic cell nuclear transfer (NT) at the blastocyst stage (NT blastocysts). Despite the predicted deficiency of the trophoblast cell lineage, we succeeded in isolating cell colonies with typical morphology of TS cells and cell lines from the NT blastocysts (ntTS cell lines) with efficiency as high as that from native blastocysts. The established 10 ntTS cell lines could be maintained in the undifferentiated state and induced to differentiate into several trophoblast subtypes in vitro. A comprehensive analysis of the transcriptional and epigenetic traits demonstrated that ntTS cells were indistinguishable from control TS cells. In addition, ntTS cells contributed exclusively to the placenta and survived until term in chimeras, indicating that ntTS cells have developmental potential as stem cells. Taken together, our data show that NT blastocysts contain cells that can produce TS cells in culture, suggesting that proper commitment to the trophoblast cell lineage in NT embryos occurs by the blastocyst stage.</p>

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  • 成体細胞の柔軟な機能維持に関わる包括的メカニズムの解明

    2023年04月
    -
    2027年03月

    小田 真由美, 基盤研究(C), 補助金,  研究代表者

  • DNA脱メチル化動的制御による心筋細胞特異的核内構造の構築と病態発生機構の解明

    2018年04月
    -
    2021年03月

    文部科学省・日本学術振興会, 科学研究費助成事業, 小田　真由美, 基盤研究（Ｃ）, 補助金,  研究代表者

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所属学協会 【 表示 ／ 非表示 】

  • 日本分子生物学会

    　

  • 日本エピジェネティクス研究会

    　
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