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Adaptive response in embryogenesis: comparative microarray analysis of gene expression in mouse fetuses.
https://repo.qst.go.jp/records/69060
https://repo.qst.go.jp/records/690604d1f55ea-89b0-4ece-a0c4-c99ae4525fe9
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2007-07-25 | |||||
| タイトル | ||||||
| タイトル | Adaptive response in embryogenesis: comparative microarray analysis of gene expression in mouse fetuses. | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_c94f | |||||
| 資源タイプ | conference object | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Vares, Guillaume
× Vares, Guillaume× Bing, Wang× Shang, Yi× Ohyama, Harumi× Tanaka, Kaoru× Nakajima, Tetsuo× Nenoi, Mitsuru× Hayata, Isamu× Ｇｕｉｌｌａｕｍｅ Ｖａｒｅｓ× 王 冰× 尚 奕× 大山 ハルミ× 田中 薫× 中島 徹夫× 根井 充× 早田 勇 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Exposure of sublethal doses of ionizing radiation can induce protective mechanisms against a subsequent higher dose irradiation. We previously demonstrated the existence of this phenomenon, called radiation-induced adaptive response (AR), in mice during late organogenesis. For better understanding of molecular mechanisms underlying AR in this model, we performed a global analysis of transcriptome regulations (14000 different genes) in cells collected from whole mouse fetuses, 24 hours after in utero exposure to priming irradiation. Several combinations of radiation dose and dose-rate were applied to induce or not an AR. While many genes were not modulated at all after radiation exposure and 166 genes were deregulated for all conditions, we identified a panel of 861 genes (so called AR genes) showing significantly different expression ratios under AR-inducing and non AR-inducing conditions. A sub-list of 119 AR genes (ARS genes) with higher discriminative characteristics was also created. We applied a functional classification algorithm which clustered AR genes in a limited number of functionally related groups. Our results emphasized the role of signal transduction mechanisms in the induction of AR. We also observed that a significant proportion of AR genes were p53-related. Furthermore, many AR genes were important for fetal development, like growth factors or genes involved in signaling cascades. Other AR-related studies suggested that priming irradiation could trigger the induction of DNA repair mechanisms. Even though no evidence of specific DNA repair modulation at the transcriptional level was observed in adapted fetuses, we studied H2AX phosphorylation kinetics following challenging irradiation in fetal liver cells and observed that H2AX phosphorylation peak appeared earlier in adapted than in non adapted cells (while disappearance rates were similar), which could indeed suggest a possible modulation of DNA repair induced by priming irradiation. However, no modulation of radiation-induced cell death by AR was described in fetal liver cells. Taken together, our results present the first evidence of molecular mechanisms modulation by AR in utero, which may have potentially important consequences for further developmental processes, and could even influence tumorigenesis. | |||||
| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 13th International Congress of Radiation Research | |||||
| 発表年月日 | ||||||
| 日付 | 2007-07-12 | |||||
| 日付タイプ | Issued | |||||
