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Disruption of homologous recombination pathway causes loss of radioresistance of moss Physcomitrella patens
https://repo.qst.go.jp/records/81246
https://repo.qst.go.jp/records/81246ce0862a3-e7c4-45c5-8540-a58b153569a3
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2020-09-14 | |||||
| タイトル | ||||||
| タイトル | Disruption of homologous recombination pathway causes loss of radioresistance of moss Physcomitrella patens | |||||
| タイトル | ||||||
| タイトル | 相同組換え経路の破綻がヒメツリガネゴケの放射線抵抗性を喪失させる | |||||
| 言語 | en | |||||
| 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 |
Yokota, Yuuichiro
× Yokota, Yuuichiro× Nogue, Fabien× Ono, Yutaka× Sakamoto, Ayako× Yokota, Yuuichiro× Ono, Yutaka× Sakamoto, Ayako |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | DNA double-strand breaks (DSBs) are one of the most severe types of DNA damage induced by ionizing radiation (IR) and other causes. We have previously found that the dose of radiation required for cell death in moss Physcomitrella patens is 100-times higher than that in mammals. We also found that, as part of its mechanism, the number of DSBs required for cell death in P. patens is 10-times more than that in mammals. This suggests that P. patens has a superior DSB repair mechanism to mammals. To elucidate the mechanism, we knockout the PpRAD51B, PpLIG4 and PpPOLQ genes, which are key genes in the homologous recombination (HR), non-homologous end joining (NHEJ) and alternative end joining (a-EJ) pathways, respectively, by the CRISPR-Cas9 or the classical recombination method. In survival tests after IR, rad51b strain was 40-times more radiosensitive than other knockout and wildtype strains. This suggests that the HR pathway but not the NHEJ and a-EJ pathways is important for the radioresistance of P. patens. Next, we measured the DSB rejoining after IR by pulsed-field gel electrophoresis. Compared with the wild-type cells, DSB rejoining was delayed in all of rad51b, lig4 and polq cells. This indicates that NHEJ and a-EJ as well as HR are involved in DSB repair. So why was the radiosensitivity significantly increased only in rad51b strain? In the wild-type, lig4 and polq cells, DSB rejoining was completed within 8 to 24 hours after IR. However, in rad51b cells, a part of the DSBs remained un-rejoined even after 24 hours. Taking together, it is suggested that failed NHEJ or a-EJ are easily bucked up by other intact pathways, but failed HR is not. | |||||
| 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 | 第４３回日本分子生物学会年会 | |||||
| 発表年月日 | ||||||
| 日付 | 2020-12-03 | |||||
| 日付タイプ | Issued | |||||
