Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada.
Proteomics. 2010 Aug;10(16):2911-26. doi: 10.1002/pmic.200900670.
Tan spot, caused by Pyrenophora tritici-repentis, is an important foliar disease of wheat. The fungus produces the host-specific, chlorosis-inducing toxin Ptr ToxB. To better understand toxin action, we examined the effects of Ptr ToxB on sensitive wheat. Photosynthesis, as measured by infrared gas analysis, declined significantly within 12 h of toxin treatment, prior to the development of chlorosis at 48-72 h. Analysis by 2-DE revealed a total of 102 protein spots with significantly altered intensities 12-36 h after toxin treatment, of which 66 were more abundant and 36 were less abundant than in the buffer-treated control. The identities of 47 of these spots were established by MS/MS, and included proteins involved in the light reactions of photosynthesis, the Calvin cycle, and the stress/defense response. Based on the declines in photosynthesis and the identities of the differentially abundant proteins, we hypothesize that Ptr ToxB causes a rapid disruption in the photosynthetic processes of sensitive wheat, leading to the generation of ROS and oxidative stress. Although the photoprotective and repair mechanisms of the host appear to initially still be functional, they are probably overwhelmed by the continued production of ROS, leading to chlorophyll photooxidation and the development of chlorosis.
叶枯病,由禾谷核腔菌引起,是小麦的一种重要叶片病害。该真菌产生对宿主具有特异性、引起黄化的毒素 Ptr ToxB。为了更好地了解毒素的作用机制,我们研究了 Ptr ToxB 对敏感型小麦的影响。通过红外线气体分析测量光合作用,在毒素处理后 12 小时内显著下降,而在 48-72 小时出现黄化之前。通过 2-DE 分析,在毒素处理 12-36 小时后共发现了 102 个蛋白斑点的强度发生了显著变化,其中 66 个比缓冲液处理的对照更丰富,36 个则更稀少。通过 MS/MS 鉴定了其中 47 个斑点的身份,这些斑点包括光合作用的光反应、卡尔文循环和应激/防御反应所涉及的蛋白。基于光合作用的下降和差异丰度蛋白的鉴定,我们假设 Ptr ToxB 导致敏感型小麦的光合作用过程迅速中断,导致 ROS 和氧化应激的产生。尽管宿主的光保护和修复机制似乎最初仍然有效,但它们可能会被持续产生的 ROS 所压倒,导致叶绿素光氧化和黄化的发展。