权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Effector gene persistence in bacterial plant pathogens

细菌植物病原体中效应基因的持久性

基本信息

批准号：
BB/R006695/1
负责人：
Dawn Arnold
金额：
$ 44.11万
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：
2018
资助国家：
英国
起止时间：
2018 至无数据
项目状态：
已结题

来源：
https://gtr.ukri.org/projects?ref=BB%2FR006695%2F1
关键词：
Effector gene persistence bacterial plant

项目摘要

The co-evolution of plant pathogens and their hosts is a complex and dynamic process. Pathogens can rapidly evolve to overcome host resistance to become virulent pathogens. This is a major cause for concern because of the threat it poses to UK and global food security. It is therefore important that we understand the causes and consequences of pathogen evolution to deliver better strategies for plant protection. In this project we aim to study the ability of plant pathogenic bacteria to overcome plant disease resistance. One of the ways that bacterial plant pathogens cause disease is to inject proteins into plant cells that inactivate plant defence mechanisms and allow them to grow inside plant tissues. These proteins are known as effector proteins. One way in which plants can protect themselves against infection is to recognise the effector proteins as they are being injected into the plant cells. If the protein is recognised the plants cells deliberately die, releasing anti-microbial chemicals, thus cutting off the source of nutrients for the bacteria and making the plant resistant to attack. However bacteria can evolve to overcome host plant resistance by losing or changing their effector genes so that the proteins they produce are not recognised by the plant. We have worked with a model bacteria-plant system that has allowed us to study in more detail how the bacteria can evolve to overcome host 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 has allowed us to study both microbial evolution and the factors that increase or decrease the durability of plant disease resistance.In the case of the Pph-bean system we have so far concentrated on the fate of one particular effector gene called avrPphB. This effector gene is interesting because it is carried on a mobile piece of DNA known as a genomic island, which can be acquired and lost by the bacteria. When the bacteria carrying this island infect a plant that is resistant, because the plant recognises avrPphB, the bacteria loses the island and can therefore go onto infect the plant without being recognised. This is an excellent example of the evolution of a pathogen to overcome host resistance. However, surprisingly, we have observed the complete loss of this effector over many experiments. Recently, using a combination of mathematical modelling and laboratory experiments, we have shown that over the course of many weeks in the resistant plant, the bacterial population will still maintain a low level of the effector gene, below the level that can be recognised by the plant, and if conditions change so the effector gene is no longer recognized, its frequency can increase. In this proposal we now aim to look in more detail at why this 'effector persistence' occurs. We will specifically study whether island and effector persistence confer any additional benefits to the bacteria. We will develop our mathematical model to provide additional insight into the basis of pathogen evolution and effector retention, and investigate whether this phenomenon is widespread. 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.

植物病原菌与寄主的协同进化是一个复杂的动态过程。病原体可以迅速进化以克服宿主抗性，成为毒性病原体。这是一个令人担忧的主要原因，因为它对英国和全球粮食安全构成威胁。因此，我们必须了解病原体进化的原因和后果，以提供更好的植物保护策略。本项目旨在研究植物病原菌克服植物抗病性的能力。细菌性植物病原体引起疾病的方式之一是将蛋白质注入植物细胞中，从而破坏植物防御机制并使它们在植物组织内生长。这些蛋白质被称为效应蛋白。植物保护自己免受感染的一种方法是在效应蛋白被注入植物细胞时识别它们。如果蛋白质被识别出来，植物细胞就会故意死亡，释放出抗微生物化学物质，从而切断细菌的营养来源，使植物能够抵抗攻击。然而，细菌可以通过失去或改变其效应基因来克服宿主植物的抗性，从而使它们产生的蛋白质不被植物识别。我们使用了一个细菌-植物系统模型，使我们能够更详细地研究细菌如何进化以克服宿主抗性。该系统使用一种称为假单胞菌pv. phaseolicola（Pph），其引起被称为晕斑病的豆类植物的重要疾病，并且使我们能够研究微生物进化和增加或减少植物抗病性的持久性的因素。这个效应基因很有趣，因为它携带在一个移动的DNA片段上，称为基因组岛，可以被细菌获得和丢失。当携带这个岛的细菌感染具有抗性的植物时，因为植物识别avrPphB，细菌失去了岛，因此可以继续感染植物而不被识别。这是一个很好的例子，说明了病原体克服宿主抗性的进化。然而，令人惊讶的是，我们在许多实验中观察到这种效应物的完全丧失。最近，使用数学建模和实验室实验的组合，我们已经表明，在抗性植物中的许多周的过程中，细菌群体仍然会保持低水平的效应基因，低于植物可以识别的水平，如果条件发生变化，效应基因不再被识别，其频率可以增加。在这个提议中，我们现在的目标是更详细地了解为什么会发生这种“效应持久性”。我们将专门研究岛和效应持久性是否赋予细菌任何额外的好处。我们将开发我们的数学模型，以提供更多的洞察病原体进化和效应保留的基础，并调查这种现象是否普遍存在。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。