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det1-1通过UVR3和PHR1光裂解酶基因的过表达诱导对UV-C的低敏感性。

det1-1-induced UV-C hyposensitivity through UVR3 and PHR1 photolyase gene over-expression.

作者信息

Castells Enric, Molinier Jean, Drevensek Stephanie, Genschik Pascal, Barneche Fredy, Bowler Chris

机构信息

Environmental and Evolutionary Genomics, CNRS UMR8197, Institut de Biologie de l'Ecole Normale Supérieure, 46 rue d'Ulm, F-75230 Paris Cedex 05, FranceInstitut de Biologie Moléculaire des Plantes du CNRS (UPR2357), conventionné avec l'Université Louis Pasteur, Strasbourg, France.

出版信息

Plant J. 2010 Aug;63(3):392-404. doi: 10.1111/j.1365-313X.2010.04249.x. Epub 2010 May 6.

DOI:10.1111/j.1365-313X.2010.04249.x
PMID:20487384
Abstract

Obligate photoautotrophs such as plants must capture energy from sunlight and are therefore exposed to the damaging collateral effects of ultraviolet (UV) irradiation, especially on DNA. Here we investigated the interconnection between light signaling and DNA repair, two concomitant pathways during photomorphogenesis, the developmental transition associated with the first light exposure. It is shown that combination of an enhanced sunscreen effect and photoreactivation confers a greater level of tolerance to damaging UV-C doses in the constitutive photomorphogenic de-etiolated1-1 (det1--1) Arabidopsis mutant. In darkness, expression of the PHR1 and UVR3 photolyase genes, responsible for photoreactivation, is maintained at a basal level through the positive action of HY5 and HYH photomorphogenesis-promoting transcription factors and the repressive effects of DET1 and COP1. Upon light exposure, HY5 and HYH activate PHR1 gene expression while the constitutively expressed nuclear-localized DET1 protein exerts a strong inhibitory effect. Altogether, the data presented indicate a dual role for DET1 in controlling expression of light-responsive and DNA repair genes, and describe more precisely the contribution of photomorphogenic regulators in the control of light-dependent DNA repair.

摘要

像植物这样的专性光合自养生物必须从阳光中捕获能量,因此会受到紫外线(UV)辐射的有害附带影响,尤其是对DNA的影响。在这里,我们研究了光信号传导与DNA修复之间的相互联系,这是光形态建成过程中的两个伴随途径,光形态建成是与首次光照相关的发育转变。结果表明,在组成型光形态建成去黄化1-1(det1-1)拟南芥突变体中,增强的防晒效应和光复活作用相结合,赋予了对破坏性UV-C剂量更高水平的耐受性。在黑暗中,负责光复活的PHR1和UVR3光解酶基因的表达通过促进光形态建成的转录因子HY5和HYH的正向作用以及DET1和COP1的抑制作用维持在基础水平。光照后,HY5和HYH激活PHR1基因表达,而组成型表达的核定位DET1蛋白则发挥强烈的抑制作用。总之,所呈现的数据表明DET1在控制光响应和DNA修复基因表达方面具有双重作用,并更精确地描述了光形态建成调节因子在光依赖性DNA修复控制中的作用。

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