Transcriptomic analysis of Cryphonectria parasitica during the initial infection stages reveals a glycoside hydrolase that is required for fungal pathogenicity

丛赤壳属 致病性 微生物学 生物 真菌生长 栗疫病 转录组 毒力 糖苷水解酶 真菌 植物 遗传学 基因 基因表达
作者
Xiaolin Qiu,Can Huang,Dianguang Xiong,Lu Yu,Yuchen Yang,Xiaorong Lin,Chengming Tian
出处
期刊:Phytopathology research [Springer Nature]
卷期号:7 (1)
标识
DOI:10.1186/s42483-025-00315-7
摘要

Abstract Chestnut blight, caused by Cryphonectria parasitica , is a notorious disease that severely harms chestnut species, leading to great economic and ecological loss worldwide. Understanding the pathogenic mechanisms of C. parasitica is crucial for developing effective disease control strategies. Therefore, screening and functional characterization of key pathogenic factors during C. parasitica and chestnut interaction are essential. Although previous studies have revealed many important virulence factors in C. parasitica , the underlying mechanisms need further study. Here, we examined the expression pattern of C. parasitica at 0, 1, 2, and 3 days post inoculation of chestnut branches (dpi) by using transcriptomic sequencing. A total of 2160 differentially expressed genes (DEGs) were identified during the infection stages compared to the uninfected control at 0 dpi. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) analyses showed significant enrichment of upregulated genes in glycoside hydrolase activity and carbohydrate metabolism pathways. Clustering analysis revealed 66 genes that were significantly upregulated with higher fold changes during the infection process, most of which were related to the degradation of the host cell wall. Additionally, 48 putative effector genes were induced during the infection stages, which were annotated as glycoside hydrolases and chitinases as well as the hydrophobic proteins, indicating the crucial roles of glycoside hydrolase during infection processes. Subsequently, we preliminary assayed the roles of a glycoside hydrolase gene CpEng1 and found that it was essential for fungal virulence. The results presented here provide a key resource for understanding the molecular basis of interaction between C. parasitica and its host.
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