柑橘目标点,由山梨假引起的,以前被认为是一种耐寒真菌病。然而,它现在已经从高纬度地区传播到温暖的低纬度地区。这里,我们对从不同地区收集的两种不同的真菌菌株进行了生理观察,并评估其致病性。有趣的是,从低纬度果园收集的CQWZ,与从高纬度果园收集的SXCG相比,表现出更高的温度耐受性和致病性。为了进一步了解这些病原体在传播过程中的温度耐受性和毒力的演变,以及这些差异背后的机制,我们进行了基因组比较分析.确定CQWZ的基因组大小为44,004,669bp,而SXCG的基因组大小被确定为45,377,339bp。通过基因组共线性分析,我们在这两个菌株的进化过程中发现了两个断点和重排。此外,基因注释结果表明,CQWZ在“外源生物生物降解和代谢”途径中拥有376个注释基因,比SXCG多79个基因。造成这种差异的主要因素是水杨酸羟化酶的存在。我们还观察到氧化应激途径和核心致病基因的变化。CQWZ显示存在热休克蛋白(HSPSSB),过氧化氢酶(CAT2),和13个核心致病基因,包括一个LysM效应器,与SXCG相比。此外,产生7种代谢物的基因簇存在显著差异,如富莫尼辛和布雷梅尔丁。最后,我们确定了监管关系,以HOG途径为核心,这可能导致耐热性和毒力的差异。随着全球气候持续变暖,作物病原体越来越多地扩展到新界。我们的发现将加深对气候变化下病原体进化机制的理解。
Citrus target spot, caused by Pseudofabraea citricarpa, was formerly considered a cold-tolerant fungal disease. However, it has now spread from high-latitude regions to warmer low-latitude regions. Here, we conducted physiological observations on two different strains of the fungus collected from distinct regions, and evaluated their pathogenicity. Interestingly, the CQWZ collected from a low-latitude orchard, exhibited higher temperature tolerance and pathogenicity when compared to the SXCG collected from a high-latitude orchard. To further understand the evolution of temperature tolerance and virulence in these pathogens during the spread process, as well as the mechanisms underlying these differences, we performed genomic comparative analysis. The genome size of CQWZ was determined to be 44,004,669 bp, while the genome size of SXCG was determined to be 45,377,339 bp. Through genomic collinearity analysis, we identified two breakpoints and rearrangements during the evolutionary process of these two strains. Moreover, gene annotation results revealed that the CQWZ possessed 376 annotated genes in the \"Xenobiotics biodegradation and metabolism\" pathway, which is 79 genes more than the SXCG. The main factor contributing to this difference was the presence of salicylate hydroxylase. We also observed variations in the oxidative stress pathways and core pathogenic genes. The CQWZ exhibited the presence of a heat shock protein (HSP SSB), a catalase (CAT2), and 13 core pathogenic genes, including a LysM effector, in comparison to the SXCG. Furthermore, there were significant disparities in the gene clusters responsible for the production of seven metabolites, such as Fumonisin and Brefeldin. Finally, we identified the regulatory relationship, with the HOG pathway at its core, that potentially contributes to the differences in thermotolerance and virulence. As the global climate continues to warm, crop pathogens are increasingly expanding to new territories. Our findings will enhance understanding of the evolution mechanisms of pathogens under climate change.