Decoding the chitin signatures generated by Xylella fastidiosa

降解几丁质的能力对真菌和细菌病原体的生存和定植成功至关重要，其中许多病原体是重要农艺学疾病的致病因子。对于缺乏几丁质的细菌性病原体，几丁质的降解在抵抗宿主定殖真菌和在其媒介中存活方面起着重要作用，如果由昆虫传播。欧洲“优先害虫名单”上的病原体之一是苛养木杆菌。这种昆虫传播的细菌是橄榄快速衰退综合征（OQDS）的原因，也是过去十年爆发的重要原因。从缺乏疾病控制来看，迫切需要了解苛养螺旋体是如何在宿主体内定殖的。以前有报道称，一种被提出的几丁质酶chiA是由X. fastidiosa分泌的，它可以将几丁质作为碳源利用，可能来自其昆虫媒介和木质部定殖真菌，ii)促进昆虫媒介的传播，iii)需要植物的全身感染，可能反对植物定殖真菌。我们的重点是chiA，因为这种细菌几丁质酶iv)在其模拟的3D结构中携带一个不寻常的环，可以确定底物特异性，并且v)可能释放几丁质低聚物，可以调节苛养X.宿主的免疫反应。虽然几丁质酶已经被研究了几十年，但我们对底物-结构-产物-生物活性的关系知之甚少，这是理解其作为毒力因子的关键。在这里，我们的目标是回答两个关键问题：苛养双歧杆菌如何降解几丁质？利用一系列确定的几丁质底物和不同的生物来源来分析甲酰胆碱的活性和特异性，将揭示降解产物，然后进行生物活性分析。结构-功能关系将探索在硅，体外和体内。2. 苛养x虫产生的几丁质低聚物的免疫调节潜能是什么？比较模型宿主和作物宿主对奇亚酸产品的不同免疫反应，以及评估模式识别受体介导的免疫，可能会为这个问题提供见解。作为一个重要的毒力因子，我们的总体目标是更好地了解chiA功能的分子细节，并阐明其在植物全身性感染中的作用。我们设想这种知识对生物技术的目的是有用的。

The ability to degrade chitin is essential for the survival and colonization success of fungal and bacterial pathogens, many of which are causal agents of agronomically-important diseases. For bacterial pathogens, which lack chitin, the degradation of chitin plays a major role in opposing host-colonizing fungi and surviving in its vector, if transmitted by insects. One of the pathogens ranked in the “list of priority pests” for Europe is Xylella fastidiosa. This insect-transmitted bacterium is the cause of the OLIVE QUICK DECLINE SYNDROME (OQDS) and important for outbreaks over the past ten years. The urgency to develop an understanding how X. fastidiosa colonizes its hosts is apparent from the lack of disease control. Previously it has been reported that a proposed chitinase, chiA, is secreted by X. fastidiosa and i) confers utilization of chitin as a carbon source, potentially from its insect vectors and xylem-colonizing fungi, ii) promotes transmission by insect vectors, and iii) is required for systemic infection in plants, maybe opposing plant-colonizing fungi. Our focus is chiA, because this bacterial chitinase iv) carries an unusual loop in its modelled 3D structure that could determine substrate specificity, and v) likely releases chitin oligomers that could modulate immune responses in hosts of X. fastidiosa. Although chitinases have been studied since decades, we have little knowledge on substrate-structure-product-bioactivity relationships, which are key to understanding its role as virulence factors. Here, our goal is to answer two key questions: 1. How does X. fastidiosa degrade chitin? Profiling chiA activity and specificity using a series of defined chitin substrates and different organismal sources will reveal degradation products then subjected to bioactivity analysis. Structure-function relationships will be explored in silico, in vitro and in vivo. 2. What is the immunomodulatory potential of chitin oligomers produced by X. fastidiosa? Comparing different immune responses to chiA products in model and crop hosts, together with assessing pattern recognition receptor-mediated immunity are likely to provide insights into this question. Being an important virulence factor, our overall aim is to better understand the molecular details of chiA function and clarify its role in systemic plant infection. We envisage that this knowledge could be useful for biotechnological purposes.