Comparative transcriptomics of two Valsa pyri isolates uncover different strategies for virulence and growth
文献类型: 外文期刊
第一作者: He, Feng
作者: He, Feng;Li, Binxin;Zhao, Yancun;Liu, Fengquan;He, Feng;Zhang, Xiong;Safdar, Asma;Ai, Gan;Kange, Alex Machio;Dou, Daolong;Li, Binxin;Cao, Haiqun
作者机构:
关键词: Valsa pyri; Virulence; Comparative transcriptomics; Cell wall degrading enzymes; Nitrogen metabolism
期刊名称:MICROBIAL PATHOGENESIS ( 影响因子:3.738; 五年影响因子:3.663 )
ISSN: 0882-4010
年卷期: 2018 年 123 卷
页码:
收录情况: SCI
摘要: Valsa pyri, an ascomycete pathogen that is a member of the Valsaceae family (Sordariomycetes, Diaporthales), which causes pear or apple canker and leads to tree death and massive yield losses. Here, we selected two V. pyri isolates (Vp14 and Vp297) that exhibited different invasion abilities for transcriptomics analyses. Compared to Vp297, Vp14 had stronger virulence and spread faster on host-like nutrients. Four samples, including mycelium or infectious mycelium, of the two isolates were sequenced. Clean reads were mapped to the V. pyri genome, and 12490 transcripts and 178 new genes were identified. There were dramatically fewer differentially expressed genes (DEGs) in Vp14 than in Vp297. According to GO and COG annotations, there were both more up- and down-regulated genes in Vp297 than in Vp14 except for genes involved in amino acid transport and metabolism, carbohydrate transport and metabolism, peroxidases and so on. Specific up-regulated DEGs, including genes encoding cell wall degrading enzymes and genes involved in nitrogen metabolism and peroxidases which play crucial roles in virulence and infectious growth, were especially enriched in Vp14. These results indicate that the Vp14 isolate may infect its host and take up nutrition more efficiently, reflecting a stronger ability for invasion or infectious growth. Our analysesindicate that a successful V. pyri infection involves multiple instances of transcriptome remodeling to regulate gene functions. Comparative transcriptomics between isolates of V. pyri may aid in our understanding of the virulence mechanism of this pathogen.
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