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Two members of the velvet family, VmVeA and VmVelB, affect conidiation, virulence and pectinase expression in Valsa mali

作者:   来源:   发布日期:2018-03-22  浏览次数:

论文信息:Yuxing Wu, Liangsheng Xu, Zhiyuan Yin, Qingqing Dai, Xiaoning Gao, Hao Feng, Ralf T. Voegele, Lili Huang. Two members of the velvet family, VmVeA and VmVelB, affect conidiation, virulence and pectinase expression in Valsa mali. Mol Plant Pathol. DOI: 10.1111/mpp.12645

JCR分区Q1,IF= 4.697 

论文摘要: Velvet protein family members are important fungal-specific regulators that are involved in conidial development, secondary metabolism, and virulence. To gain broader insight into the physiological functions into the velvet protein family of Valsa mali, which causes a highly destructive canker disease on apple, we conducted a functional analysis of two Velvet protein family members (VmVeA and VmVelB) via gene replacement strategy. Deletion mutants of VmVeA and VmVelB showed increased melanin production, conidiation, and sensitivity to abiotic stresses, but exhibited reduced virulence on detached apple leaves and twigs. Further studies demonstrated that the regulation of conidiation by VmVeA or VmVelB was positively correlated with melanin synthesis transcription factor VmCmr1. More importantly, transcript levels of pectinase genes were shown to be decreased in deletion mutants compared to those of the wild type during infection. However, the expression of other cell wall-degrading enzymes including cellulase, hemi-cellulase, or ligninase genes was not affected in the deletion mutants. Furthermore, the determination of pectinase activity and immunogold labeling of pectin demonstrated that the capacity of pectin degradation was attenuated due to deletions of VmVeA and VmVelB. Finally, the interaction of VmVeA with VmVelB was identified through co-immunoprecipitation assays. VmVeA and VmVelB play critical roles in conidiation and virulence likely by regulating melanin synthesis transcription factor VmCmr1 and affecting pectinase gene expression in V. mali, respectively.

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