...
首页> 外文期刊>American Journal of Plant Sciences >Tomato Plants Overexpressing a Celery Mannitol Dehydrogenase (MTD) Have Decreased Susceptibility to Botrytis cinerea
【24h】

Tomato Plants Overexpressing a Celery Mannitol Dehydrogenase (MTD) Have Decreased Susceptibility to Botrytis cinerea

机译:过量表达芹菜甘露醇脱氢酶(MTD)的番茄植株对灰葡萄孢的敏感性降低

获取原文
   

获取外文期刊封面封底 >>

       

摘要

The oxidative burst is a critical early event in plant-pathogen interactions that leads to a localized, programmed cell death (PCD) called the hypersensitive response (HR). The HR and associated PCD retard infection by biotrophic pathogens, but can, in fact, enhance infection by necrotrophic pathogens like Botrytis cinerea. In addition to signaling the induction of the HR, reactive oxygen species (ROS) produced during the oxidative burst are?antimicrobial. We hypothesize that pathogens such as B. cinerea survive the antimicrobial effects of ROS, at least partially by secreting the antioxidant mannitol during infection. This is supported by the previous observation that overexpression of the catabolic enzyme mannitol dehydrogenase (MTD) can decrease a plants susceptibility to mannitol-secreting pathogens like B. cinerea. To extend the above hypothesis, and test the general utility of this approach in an important horticultural crop, we overexpressed celery MTD in tomato (Solanum lycopersicum cv. “Moneymaker”). In these studies, we observed a significant increase (up to 90%) in resistance to B. cinerea in transgenic tomatoes expressing high amounts of MTD.
机译:氧化爆发是植物-病原体相互作用中的关键早期事件,会导致局部程序性细胞死亡(PCD),称为超敏反应(HR)。 HR和相关的PCD阻止了生物营养性病原体的感染,但实际上可以增强坏死性病原体(如灰葡萄孢)的感染。除了发出HR信号外,氧化爆发过程中产生的活性氧(ROS)也具有抗菌作用。我们假设病原体,例如灰质芽孢杆菌(B. cinerea)在感染过程中至少部分地通过分泌抗氧化剂甘露醇而幸免于ROS的抗菌作用。以前的观察结果支持了这一点,即分解代谢酶甘露醇脱氢酶(MTD)的过表达可以降低植物对分泌甘露醇的病原体(如灰质芽孢杆菌)的敏感性。为了扩展上述假设,并测试这种方法在重要的园艺作物中的通用性,我们在番茄(Solanum lycopersicum cv。“ Moneymaker”)中过表达了芹菜MTD。在这些研究中,我们观察到在表达大量MTD的转基因番茄中对灰葡萄孢的抗性显着提高(最高90%)。

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