Effector gene persistence in bacterial plant pathogens

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的抵抗力，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食品安全构成了威胁。因此，我们必须了解病原体进化的原因和后果，以便为植物保护提供更好的策略。在这个项目中，我们旨在研究植物致病菌克服植物抗病的能力。植物细菌性病原体致病的方式之一是将蛋白质注入植物细胞，使植物的防御机制失活，并允许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。如果这种蛋白质被识别出来，植物细胞就会故意死亡，释放出抗微生物的化学物质，从而切断细菌的营养来源，使植物抵抗攻击。然而，细菌可以通过失去或改变它们的效应基因来进化以克服寄主植物的抗性，从而使它们产生的蛋白质不被植物识别。我们研究了一个模型细菌-植物系统，这使我们能够更详细地研究细菌如何进化以克服宿主的抗性。这个系统使用一种叫做丁香假单胞菌pv的细菌。这使得我们能够研究微生物的进化以及增加或减少植物抗病持久性的因素。就ph-bean系统而言，到目前为止，我们关注的是一种名为avrPphB的特定效应基因的命运。这种效应基因很有趣，因为它携带在被称为基因组岛的可移动DNA片段上，它可以被细菌获得和丢失。当携带这个岛的细菌感染一株具有抗性的植物时，因为植物识别avrPphB，细菌失去了这个岛，因此可以在不被识别的情况下感染植物。这是病原体进化以克服宿主耐药性的一个极好的例子。然而，令人惊讶的是，我们在许多实验中观察到这种效应完全消失。最近，利用数学模型和实验室实验的结合，我们已经表明，在抗性植物的许多周过程中，细菌种群仍将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，使效应基因不再被识别，其频率可以增加。在本提案中，我们现在的目标是更详细地研究为什么会出现这种“效应持久性”。我们将专门研究孤岛和效应持久性是否会给细菌带来任何额外的好处。我们将开发我们的数学模型，以提供对病原体进化和效应物保留的基础的额外见解，并调查这种现象是否普遍存在。这项研究将有助于阐明支持细菌致病性进化和作物植物抗病能力崩溃的基本机制，为将来可能用于改进用于对抗致病微生物的疾病管理策略提供知识。

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.