The Mycobacterium marinum mel2 locus displays similarity to bacterial bioluminescence systems and plays a role in defense against reactive oxygen and nitrogen species.

The Mycobacterium marinum mel2 locus displays similarity to bacterial bioluminescence systems and plays a role in defense against reactive oxygen and nitrogen species.
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DOI:
10.1186/1471-2180-7-4
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发表时间:
2007-01-19
期刊:
影响因子:
4.2
通讯作者:
Cirillo JD
Cirillo JD
中科院分区:
生物学3区
文献类型:
--
作者:
Subbian S;Mehta PK;Cirillo SL;Cirillo JD

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分枝杆菌已经开发了许多途径,提供部分保护,防止活性氧(ROS)和活性氮(RNS)。我们最近确定了一个位点在海洋分枝杆菌,梅尔2,在感染巨噬细胞的过程中发挥作用。mel 2作用的分子机制还没有很好地理解。为了更好地理解M的作用。marinummel2基因座,我们在计算机中检测了这些基因的保守基序。在mel2基因座和其他细菌物种中编码生物发光的基因座之间观察到惊人的相似性。由于生物发光系统可以在抗氧化应激中发挥作用,我们推测mel2位点可能对分枝杆菌对ROS和RNS的抗性很重要。我们发现一个M。在这个假定的操纵子melF中的第一个基因中的marinum突变体赋予对ROS和RNS两者的增加的易感性。该突变体对ROS和RNS一起比单独的任一反应性物种更敏感。这些观察结果支持了M. marinum mel2基因座在抗氧化应激中的作用,并提供了生物发光系统可能从氧化防御机制进化而来的额外证据。
Mycobacteria have developed a number of pathways that provide partial protection against both reactive oxygen species (ROS) and reactive nitrogen species (RNS). We recently identified a locus in Mycobacterium marinum, mel2, that plays a role during infection of macrophages. The molecular mechanism of mel2 action is not well understood. To better understand the role of the M. marinum mel2 locus, we examined these genes for conserved motifs in silico. Striking similarities were observed between the mel2 locus and loci that encode bioluminescence in other bacterial species. Since bioluminescence systems can play a role in resistance to oxidative stress, we postulated that the mel2 locus might be important for mycobacterial resistance to ROS and RNS. We found that an M. marinum mutant in the first gene in this putative operon, melF, confers increased susceptibility to both ROS and RNS. This mutant is more susceptible to ROS and RNS together than either reactive species alone. These observations support a role for the M. marinum mel2 locus in resistance to oxidative stress and provide additional evidence that bioluminescence systems may have evolved from oxidative defense mechanisms.
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