Characterization of T-DNA insertion mutants and RNAi silenced plants of Arabidopsis thaliana UV-damaged DNA binding protein 2 (AtUV-DDB2)

Characterization of T-DNA insertion mutants and RNAi silenced plants of Arabidopsis thaliana UV-damaged DNA binding protein 2 (AtUV-DDB2)
复制标题

DOI:
10.1007/s11103-006-6408-z
复制
发表时间:
2006-05-01
影响因子:
5.1
通讯作者:
Sakaguchi, Kengo
Sakaguchi, Kengo
中科院分区:
生物学2区
文献类型:
--
作者:
Koga, Asami;Ishibashi, Toyotaka;Sakaguchi, Kengo

文献摘要

被引文献

相似文献

人紫外线损伤DNA结合蛋白(UV-DDB)是一种由127 kDa(UV-DDB 1)和48 kDa(UV-DDB 2)亚基组成的异二聚体蛋白,已被证明参与DNA修复。为了阐明植物UV-DDB 2在体内的功能,我们分析了拟南芥UV-DDB 2亚基的T-DNA插入突变体(atuv-ddb 2突变体)和AtUV-DDB 2 RNAi沉默植物(atuv-ddb 2沉默植物)。atuv-ddb 2突变体和atuv-ddb 2沉默的植物都能存活,这表明AtUV-DDB 2对于生存不是必需的。有趣的是,两种植物类型都表现出矮化表型,这意味着分生组织的生长受损。据我们所知,这是第一次在植物或动物中发现矮表型与UV-DDB 2突变相关。突变体还表现出对UV照射、甲磺酸甲酯和过氧化氢处理的敏感性增加,表明AtUV-DDB 2也参与DNA修复。我们的研究结果表明,AtUV-DDB 2不仅在DNA修复中起作用,而且对植物分生组织中的细胞增殖也有直接或间接的影响。
The human UV-damaged DNA binding protein (UV-DDB), a heterodimeric protein composed of 127 kDa (UV-DDB1) and 48 kDa (UV-DDB2) subunits, has been shown to be involved in DNA repair. To elucidate the in vivo function of plant UV-DDB2, we have analyzed T-DNA insertion mutants of the Arabidopsis thaliana UV-DDB2 subunit (atuv-ddb2 mutants) and AtUV-DDB2 RNAi silenced plants (atuv-ddb2 silenced plants). atuv-ddb2 mutants and atuv-ddb2 silenced plants were both viable, suggesting that AtUV-DDB2 is not essential for survival. Interestingly, both plant types showed a dwarf phenotype, implying impaired growth of the meristem. To the best of our knowledge, this is the first occasion that a dwarf phenotype has been found to be associated with a UV-DDB2 mutation in either plants or animals. The mutants also demonstrated increased sensitivity to UV irradiation, methyl methanesulfonate and hydrogen peroxide treatment, indicating that AtUV-DDB2 is also involved in DNA repair. Our results lead us to suggest that not only does AtUV-DDB2 function in DNA repair, it also has a direct or indirect influence on cell proliferation in the plant meristem.