欺骗警卫:利用植物防御来对疾病敏感性进行利用
J Lorang1, T Kidarsa, C S Bradford
1Department of Botany and Plant Pathology and Center for Genome Research and Biocomputing, Oregon State University, Corvallis, OR 97331, USA.
概括
病原体使用效应剂来抑制植物的防御. 在一个令人惊的转折中,Cochliobolus victoriae真菌使用维克托林来激活植物易感性蛋白 (LOV1),导致Arabidopsis植物的疾病.
科学领域:
- 植物病理学 植物病理学
- 分子植物微生物相互作用.
- 植物免疫力 植物免疫力
背景情况:
- 病原体通常分泌效应物以克服宿主植物的防御.
- 植物使用耐药性蛋白来检测病原体效应因子并激活防御反应.
- 病原体效应因子和植物耐药性蛋白之间的相互作用对于确定疾病结果至关重要.
研究的目的:
- 为了研究一种新的机制,即菌Cochliobolus victoriae操纵植物防御途径.
- 阐明维克托林,TRX-h5和LOV1在植物病原体相互作用中的作用.
- 了解病原体效应因子如何矛盾地诱导易感性.
主要方法:
- 研究了维克托林,铁素 (TRX-h5) 和阿拉比多普西斯敏感性蛋白LOV1.1之间的相互作用.
- 利用缺乏LOV1的阿拉比多普西斯突变体来评估这种蛋白质在疾病发展中的作用.
- 分析了维克托林与TRX-h5结合在LOV1.1存在或不存在时的生物化学和细胞后果.
主要成果:
- 在没有LOV1的情况下,维克托林会抑制TRX-h5,从而损害植物的防御能力,而不会引起疾病.
- 在LOV1的存在下,与TRX-h5结合的维克托林激活LOV1,引发一种类似于抵抗的反应,这具有悖论性地赋予了易感性.
- 这种相互作用表明了一种独特的策略,在这种策略中,病原体效应者利用植物自身的防护机制来引起疾病.
结论:
- 植物易感性蛋白LOV1在调解对Cochliobolus victoriae.疾病易感性方面发挥着至关重要的作用.
- 维克托林通过劫持植物的防御系统,特别是通过激活LOV1.1,作为毒性效应剂.
- 这项研究揭示了一种新的病原体毒性机制,其中防御激活导致易感性.
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