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Understanding how plant antimicrobial "hot zones" can accelerate pathogen evolution

了解植物抗菌“热区”如何加速病原体进化

基本信息

批准号：
BB/J014796/1
负责人：
Dawn Arnold
金额：
$ 32.54万
依托单位：
University of the West of England
依托单位国家：
英国
项目类别：
Research Grant
财政年份：
2013
资助国家：
英国
起止时间：
2013 至无数据
项目状态：
已结题

来源：
https://gtr.ukri.org/projects?ref=BB%2FJ014796%2F1
关键词：
Understanding how plant antimicrobial hot

项目摘要

Gone are the days of food mountains whereby agricultural policies and crop production resulted in large stocks of food. Instead, the world is facing a major challenge to produce enough food to feed a growing population. Food security is a major global research priority and we know that we must double our food production within the next 20 years just to keep pace with population increases. To do this requires improvements in many aspects of food production. One of the major areas for improvement is preventing crop loss due to plant disease.Most of the microorganisms that cause plant disease are engaged in a constant arms race with plants such that microorganisms are rapidly evolving to infect disease resistant plants while plants are evolving to resist pathogen attack. In an agricultural setting, plant breeders face the increasingly difficult challenge of developing new disease-resistant varieties to replace those rendered ineffective due to microbial evolution. To prolong the usefulness of disease resistant plant varieties, and to reduce the rate at which microorganisms overcome disease resistance, it is imperative that we fully understand how microorganisms evolve and the drivers of this evolution. We have developed a model system for understanding microbial evolution to overcome plant disease resistance. This system uses a bacterium called Pseudomonas syringae pv. phaseolicola (Pph), which causes an important disease of bean plants known as halo blight, and represents an excellent system for studying both microbial evolution and the factors that increase or decrease the durability of plant disease resistance.In the case of Pph and bean, the plant has developed mechanisms to recognise specific strains of Pph, and so resist invasion. In this dynamic system the bacterium has a number of ways of changing its genome, and therefore the proteins it expresses, in order to evade plant recognition. Alterations in the structure or production of bacterial proteins may prevent their detection by potential host plants and allow the bacteria to grow within the plant. We have shown that changes in the genome of Pph allow this bacterium to overcome plant disease resistance. Certain strains of Pph carry a gene that produces a protein the plant can detect as belonging to Pph, alerting it to trigger its defence systems and prevent Pph growth. The gene for this protein lies within a discrete region of the Pph genome known as a genomic island. To counter plant recognition, Pph removes the genomic island from its chromosome such that daughter cells no longer have the island. Interestingly, we observed that this dramatic change in Pph occurs most frequently in infection site "hot zones" in resistant varieties of bean. These hot zones generate highly antimicrobial conditions following bacterial invasion. Therefore the chemical changes that occur in resistant plants actually accelerate the evolution of a more virulent form of the pathogen.More recently we have also shown that bacteria growing in plant tissue can become competent to take up foreign DNA in a process called transformation. This acquisition of new genes could allow Pph to gain an advantage in the fight between the plant and the bacterium. In this proposal we aim to study the chemical composition of the "hot zone" to understand which factors are responsible for inducing gene loss and gene gain in Pph. We also aim to identify the genes responsible for DNA uptake in the bacteria, and to understand how signals present in the "hot zone" cause increased DNA uptake in Pph. This research will help to elucidate the fundamental mechanisms underpinning the evolution of bacterial pathogenicity and the breakdown of disease resistance in crop plants, providing knowledge that, in the future, may be used to improve the disease management strategies used against disease-causing microorganisms.

农业政策和作物生产导致大量粮食库存的粮食山时代已经一去不复返了。相反，世界正面临着一个重大挑战，即生产足够的粮食来养活不断增长的人口。粮食安全是一个主要的全球研究优先事项，我们知道，我们必须在未来20年内将粮食产量翻一番，才能跟上人口增长的步伐。要做到这一点，需要在粮食生产的许多方面进行改进。大多数引起植物病害的微生物与植物进行持续的军备竞赛，使得微生物快速进化以感染抗病植物，而植物进化以抵抗病原体攻击。在农业环境中，植物育种者面临着越来越困难的挑战，即开发新的抗病品种，以取代那些由于微生物进化而变得无效的品种。为了延长抗病植物品种的有效性，并降低微生物克服抗病性的速度，我们必须充分了解微生物如何进化以及这种进化的驱动因素。我们已经开发了一个模型系统，用于了解微生物进化以克服植物抗病性。该系统使用一种称为假单胞菌pv. phaseolicola（Pph）是菜豆的一种重要病害，它引起菜豆的晕斑病，是研究微生物进化和提高或降低植物抗病性持久性的因素的一个很好的系统。在Pph和菜豆的情况下，植物已经发展出识别Pph特定菌株的机制，从而抵抗入侵。在这个动态系统中，细菌有多种方式改变其基因组，从而改变其表达的蛋白质，以逃避植物识别。细菌蛋白质的结构或生产的改变可能会阻止它们被潜在的宿主植物检测到，并允许细菌在植物内生长。我们已经证明，Pph基因组的变化使这种细菌能够克服植物抗病性。某些Pph菌株携带一种基因，该基因产生一种蛋白质，植物可以检测到属于Pph，提醒它触发防御系统并阻止Pph生长。这种蛋白质的基因位于Pph基因组的一个离散区域内，称为基因组岛。为了对抗植物识别，Pph将基因组岛从其染色体上移除，使得子细胞不再具有岛。有趣的是，我们观察到，这种戏剧性的变化，在Pph最经常发生在感染部位的“热区”的抗性品种的豆类。这些热区在细菌入侵后产生高度抗菌的条件。因此，抗性植物中发生的化学变化实际上加速了病原体毒性更强形式的进化。最近，我们还表明，在植物组织中生长的细菌可以在一个称为转化的过程中变得有能力吸收外来DNA。这种新基因的获得可以使Pph在植物和细菌之间的斗争中获得优势。在这个建议中，我们的目标是研究“热区”的化学成分，以了解哪些因素是负责诱导Pph的基因丢失和基因获得。我们的目标还包括确定细菌中负责DNA摄取的基因，并了解“热区”中存在的信号如何导致Pph中DNA摄取增加。这项研究将有助于阐明细菌致病性进化和作物抗病性崩溃的基本机制，提供知识，在未来，可用于改善针对致病微生物的疾病管理策略。