VeA Is Associated with the Response to Oxidative Stress in the Aflatoxin Producer Aspergillus flavus
VeA Is Associated with the Response to Oxidative Stress in the Aflatoxin Producer Aspergillus flavus
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DOI：
10.1128/ec.00099-14
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发表时间：
2014-08-01
期刊：
影响因子：
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通讯作者：
Calvo, Ana M.
中科院分区：
文献类型：
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作者：
Baidya, Sachin;Duran, Rocio M.;Calvo, Ana M.
真菌物种的生存取决于这些生物体对环境压力的反应能力。渗透胁迫或高水平的活性氧（ROS）可引起真菌中的胁迫，从而导致生长抑制。真核细胞和原核细胞都已经开发出许多机制来抵抗ROS存在下的应激并存活下来。在许多真菌中，HOG信号通路对于氧化应激反应以及渗透应激反应是至关重要的。这项研究表明，虽然渗透应激反应只受到主调节因子veA的轻微影响，但该基因也已知控制许多真菌物种的形态发育和次级代谢，对黄曲霉毒素产生真菌的氧化应激反应具有深远影响。黄曲霉。我们发现A.参与HOG信号通路的黄曲霉同源基因受veA调节。缺失veA导致暴露于过氧化氢后氧化应激反应基因的转录水平降低。此外，分析VeA对cat 1和trxB启动子的影响表明，VeA的存在改变了DNA-蛋白质复合物的形成。这是特别值得注意的cat 1启动子，其中VeA的情况下，在异常更强的复合物的形成与减少cat 1的表达和更敏感的ROS在一个veA缺失突变体，表明VeA可能会阻止负转录调节剂的cat 1启动子的结合。我们的研究还表明，veA积极影响的转录因子基因atfB的表达，并在cat 1启动子的DNA-蛋白质复合物的正常形成是依赖于AtfB。
Survival of fungal species depends on the ability of these organisms to respond to environmental stresses. Osmotic stress or high levels of reactive oxygen species (ROS) can cause stress in fungi resulting in growth inhibition. Both eukaryotic and prokaryotic cells have developed numerous mechanisms to counteract and survive the stress in the presence of ROS. In many fungi, the HOG signaling pathway is crucial for the oxidative stress response as well as for osmotic stress response. This study revealed that while the osmotic stress response is only slightly affected by the master regulator veA, this gene, also known to control morphological development and secondary metabolism in numerous fungal species, has a profound effect on the oxidative stress response in the aflatoxin-producing fungus Aspergillus flavus. We found that the expression of A. flavus homolog genes involved in the HOG signaling pathway is regulated by veA. Deletion of veA resulted in a reduction in transcription levels of oxidative stress response genes after exposure to hydrogen peroxide. Furthermore, analyses of the effect of VeA on the promoters of cat1 and trxB indicate that the presence of VeA alters DNA-protein complex formation. This is particularly notable in the cat1 promoter, where the absence of VeA results in abnormally stronger complex formation with reduced cat1 expression and more sensitivity to ROS in a veA deletion mutant, suggesting that VeA might prevent binding of negative transcription regulators to the cat1 promoter. Our study also revealed that veA positively influences the expression of the transcription factor gene atfB and that normal formation of DNA-protein complexes in the cat1 promoter is dependent on AtfB.