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RAD54在活植物细胞中响应DNA损伤时形成DNA修复病灶。

RAD54 forms DNA repair foci in response to DNA damage in living plant cells.

作者信息

Hirakawa Takeshi, Hasegawa Junko, White Charles I, Matsunaga Sachihiro

机构信息

Department of Applied Biological Science, Faculty of Science and Technology, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba, 278-8510, Japan.

Génétique, Reproduction et Développement, UMR CNRS 6293, Clermont Université, INSERM U1103, Université Blaise Pascal, Clermont-Ferrand, France.

出版信息

Plant J. 2017 Apr;90(2):372-382. doi: 10.1111/tpj.13499. Epub 2017 Mar 25.

DOI:10.1111/tpj.13499
PMID:28155243
Abstract

Plants have various defense mechanisms against environmental stresses that induce DNA damage. Genetic and biochemical analyses have revealed the sensing and signaling of DNA damage, but little is known about subnuclear dynamics in response to DNA damage in living plant cells. Here, we observed that the chromatin remodeling factor RAD54, which is involved in DNA repair via the homologous recombination pathway, formed subnuclear foci (termed RAD54 foci) in Arabidopsis thaliana after induction of DNA double-strand breaks. The appearance of RAD54 foci was dependent on the ATAXIA-TELANGIECTASIA MUTATED-SUPPRESSOR OF GAMMA RESPONSE 1 pathway, and RAD54 foci were co-localized with γH2AX signals. Laser irradiation of a subnuclear area demonstrated that in living cells RAD54 was specifically accumulated at the damaged site. In addition, the formation of RAD54 foci showed specificity for cell type and region. We conclude that RAD54 foci correspond to DNA repair foci in A. thaliana.

摘要

植物具有多种抵御诱导DNA损伤的环境胁迫的防御机制。遗传和生化分析揭示了DNA损伤的感知和信号传导,但对于活植物细胞中响应DNA损伤的核内亚动态知之甚少。在这里,我们观察到参与通过同源重组途径进行DNA修复的染色质重塑因子RAD54,在拟南芥中诱导DNA双链断裂后形成核内亚结构域(称为RAD54结构域)。RAD54结构域的出现依赖于共济失调毛细血管扩张突变型-γ反应1抑制因子途径,并且RAD54结构域与γH2AX信号共定位。对核内亚区域的激光照射表明,在活细胞中RAD54特异性地积累在受损部位。此外,RAD54结构域的形成表现出对细胞类型和区域的特异性。我们得出结论,RAD54结构域对应于拟南芥中的DNA修复结构域。

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