...
首页> 外文期刊>Toxins >Loss of msnA, a Putative Stress Regulatory Gene, in Aspergillus parasiticus and Aspergillus flavus Increased Production of Conidia, Aflatoxins and Kojic Acid
【24h】

Loss of msnA, a Putative Stress Regulatory Gene, in Aspergillus parasiticus and Aspergillus flavus Increased Production of Conidia, Aflatoxins and Kojic Acid

机译:寄生曲霉和黄曲霉中假定的压力调节基因msnA的缺失增加了分生孢子,黄曲霉毒素和曲酸的产量

获取原文
   

获取外文期刊封面封底 >>

       

摘要

Production of the harmful carcinogenic aflatoxins by Aspergillus parasiticus and Aspergillus flavus has been postulated to be a mechanism to relieve oxidative stress. The msnA gene of A. parasiticus and A. flavus is the ortholog of Saccharomyces cerevisiae MSN2 that is associated with multi-stress response. Compared to wild type strains, the msnA deletion (∆msnA) strains of A. parasiticus and A. flavus exhibited retarded colony growth with increased conidiation. The ∆msnA strains also produced slightly higher amounts of aflatoxins and elevated amounts of kojic acid on mixed cereal medium. Microarray assays showed that expression of genes encoding oxidative stress defense enzymes, i.e., superoxide dismutase, catalase, and cytochrome c peroxidase in A. parasiticus ∆msnA, and the catalase A gene in A. flavus ∆msnA, was up-regulated. Both A. parasiticus and A. flavus ∆msnA strains produced higher levels of reactive oxygen species (ROS), and ROS production of A. flavus msnA addback strains was decreased to levels comparable to that of the wild type A. flavus. The msnA gene appears to be required for the maintenance of the normal oxidative state. The impairment of msnA resulted in the aforementioned changes, which might be used to combat the increased oxidative stress in the cells.
机译:假定由寄生曲霉和黄曲霉产生有害的致癌性黄曲霉毒素是缓解氧化应激的机制。寄生曲霉和黄曲霉的msnA基因是酿酒酵母MSN2的直系同源基因,与多应激反应有关。与野生型菌株相比,寄生曲霉和黄曲霉的msnA缺失菌株(ΔmsnA)表现出随着分生孢子数增加而延迟的菌落生长。在混合谷物培养基上,∆msnA菌株还产生了较高量的黄曲霉毒素和较高的曲酸。微阵列分析显示,在拟南芥∆msnA中编码氧化应激防御酶即超氧化物歧化酶,过氧化氢酶和细胞色素c过氧化物酶的基因以及在黄曲霉∆msnA中过氧化氢酶A基因的表达均被上调。寄生寄生曲霉和黄曲霉ΔmsnA菌株均产生较高水平的活性氧(ROS),而黄曲霉msnA加回菌株的ROS产量降低至与野生型黄曲霉相当的水平。 msnA基因似乎是维持正常氧化状态所必需的。 msnA的损伤导致上述变化,可用于抵抗细胞中增加的氧化应激。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号