DdrA, DdrD, and PprA: components of UV and mitomycin C resistance in Deinococcus radiodurans R1.
DdrA, DdrD, and PprA: components of UV and mitomycin C resistance in Deinococcus radiodurans R1.
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DOI：
10.1371/journal.pone.0069007
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Battista JR
中科院分区：
文献类型：
--
作者：
Selvam K;Duncan JR;Tanaka M;Battista JR
通过删除耐辐射奇球菌R1的ddrA、ddrB、ddrC、ddrD和pprA基因座以及所有可能的基因对组合而产生的突变体显示，编码的基因产物有助于该物种对紫外线和/或丝裂霉素C的抗性。从其他野生型细胞中删除pprA会使所得菌株对UV照射敏感，相对于R1，活力降低多达8倍。如果将这种缺失引入ΔddrA或ΔddrD背景中，所产生的菌株对紫外线的致死效应变得非常敏感。在1000 Jm-2的能量密度下，ΔddrA ΔpprA和ΔddrD ΔpprA菌株对UV的敏感性分别是仅丢失pprA菌株的100倍和1000倍。缺失ddrA导致菌株对丝裂霉素C的敏感性增加100倍，但联合收割机缺失ddrA与缺失ddrC或ddrD组合的背景中，丝裂霉素抗性恢复至野生型水平。ddrB的失活也增加了D.在一些实施方案中，ΔddrB背景中缺失ddrC或ddrD的ddrA突变体进一步增加了耐放射性铀对丝裂霉素的敏感性，但与ddrA突变体不同，从ΔddrB背景中缺失ddrC或ddrD进一步增加了该敏感性。尽管这些基因产物的损失对DNA损伤抗性的影响，似乎没有直接影响切除修复或同源重组，这表明它们参与了新的过程，促进耐受紫外线和链间交联在这个物种。
Mutants created by deleting the ddrA, ddrB, ddrC, ddrD, and pprA loci of Deinococcus radiodurans R1alone and in all possible combinations of pairs revealed that the encoded gene products contribute to this species’ resistance to UV light and/or mitomycin C. Deleting pprA from an otherwise wild type cell sensitizes the resulting strain to UV irradiation, reducing viability by as much as eight fold relative to R1. If this deletion is introduced into a ΔddrA or ΔddrD background, the resulting strains become profoundly sensitive to the lethal effects of UV light. At a fluence of 1000 Jm-2, the ΔddrA ΔpprA and ΔddrD ΔpprA strains are 100- and 1000-fold more sensitive to UV relative to the strain that has only lost pprA. Deletion of ddrA results in a 100 fold increase in strain sensitivity to mitomycin C, but in backgrounds that combine a deletion of ddrA with deletions of either ddrC or ddrD, mitomycin resistance is restored to wild type levels. Inactivation of ddrB also increases D. radiodurans sensitivity to mitomycin, but unlike the ddrA mutant deleting ddrC or ddrD from a ΔddrB background further increases that sensitivity. Despite the effect that loss of these gene products has on DNA damage resistance, none appear to directly affect either excision repair or homologous recombination suggesting that they participate in novel processes that facilitate tolerance to UV light and interstrand crosslinks in this species.
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影响因子：
3.2
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