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耐辐射球菌对镉毒性的全基因组响应。

Genome-wide response of Deinococcus radiodurans on cadmium toxicity.

机构信息

Radiation Research Division for Biotechnology, Korea Atomic Energy Research Institute, Jeongeup 580-185, Republic of Korea.

出版信息

J Microbiol Biotechnol. 2011 Apr;21(4):438-47.

PMID:21532329
Abstract

Deinococcus radiodurans is extremely resistant to various genotoxic conditions and chemicals. In this study, we characterized the effect of a sublethal concentration (100 microM) of cadmium (Cd) on D. radiodurans using a whole-genome DNA microarray. Time-course global gene expression profiling showed that 1,505 genes out of 3,116 total ORFs were differentially expressed more than 2-fold in response to Cd treatment for at least one timepoint. The majority of the upregulated genes are related to iron uptake, cysteine biosynthesis, protein disulfide stress, and various types of DNA repair systems. The enhanced upregulation of genes involved in cysteine biosynthesis and disulfide stress indicate that Cd has a high affinity for sulfur compounds. Provocation of iron deficiency and growth resumption of Cd-treated cells by iron supplementation also indicates that CdS forms in iron-sulfur-containing proteins such as the [Fe-S] cluster. Induction of base excision, mismatch, and recombinational repair systems indicates that various types of DNA damage, especially base excision, were enhanced by Cd. Exposure to sublethal Cd stress reduces the growth rate, and many of the downregulated genes are related to cell growth, including biosynthesis of cell membrane, translation, and transcription. The differential expression of 52 regulatory genes suggests a dynamic operation of complex regulatory networks by Cd-induced stress. These results demonstrate the effect of Cd exposure on D. radiodurans and how the related genes are expressed by this stress.

摘要

耐辐射球菌对各种遗传毒性条件和化学物质具有极强的抗性。在这项研究中,我们使用全基因组 DNA 微阵列来研究亚致死浓度(100μM)的镉(Cd)对耐辐射球菌的影响。时间过程全基因表达谱分析显示,在 Cd 处理至少一个时间点后,3116 个总 ORF 中有 1505 个基因的表达水平差异超过 2 倍。上调基因的大多数与铁摄取、半胱氨酸生物合成、蛋白质二硫键应激和各种类型的 DNA 修复系统有关。半胱氨酸生物合成和二硫键应激相关基因的增强上调表明 Cd 对硫化合物具有高亲和力。通过补充铁来引发铁缺乏和恢复 Cd 处理细胞的生长也表明 CdS 形成于含铁硫的蛋白质中,如[Fe-S]簇。碱基切除、错配和重组修复系统的诱导表明,各种类型的 DNA 损伤,尤其是碱基切除,都被 Cd 增强了。暴露于亚致死 Cd 应激会降低生长速度,许多下调的基因与细胞生长有关,包括细胞膜、翻译和转录的生物合成。52 个调节基因的差异表达表明,复杂的调控网络在 Cd 诱导的应激下动态运作。这些结果表明了 Cd 暴露对耐辐射球菌的影响以及相关基因如何通过这种应激表达。

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