A systematic analysis of apple root resistance traits to Pythium ultimum infection and the underpinned molecular regulations of defense activation

对苹果根系抗终极腐霉菌感染的性状及其防御激活的分子调控机制进行系统分析

阅读:1

Abstract

Apple replant disease (ARD), caused by a pathogen complex, significantly impacts apple orchard establishment. The molecular regulation on ARD resistance has not been investigated until recently. A systematic phenotyping effort and a series of transcriptomic analyses were performed to uncover the underpinned molecular mechanism of apple root resistance to P. ultimum, a representative member in ARD pathogen complex. Genotype-specific plant survival rates and biomass reduction corresponded with microscopic features of necrosis progression patterns along the infected root. The presence of defined boundaries separating healthy and necrotic sections likely caused delayed necrosis expansion in roots of resistant genotypes compared with swift necrosis progression and profuse hyphae growth along infected roots of susceptible genotypes. Comprehensive datasets from a series of transcriptome analyses generated the first panoramic view of genome-wide transcriptional networks of defense activation between resistant and susceptible apple roots. Earlier and stronger molecular defense activation, such as pathogen perception and hormone signaling, may differentiate resistance from susceptibility in apple root. Delayed and interrupted activation of multiple defense pathways could have led to an inadequate resistance response. Using the panel of apple rootstock germplasm with defined resistant and susceptible phenotypes, selected candidate genes are being investigated by transgenic manipulation including CRISPR/Cas9 tools for their specific roles during apple root defense toward P. ultimum infection. Individual apple genes with validated functions regulating root resistance responses can be exploited for developing molecular tools for accurate and efficient incorporation of resistance traits into new apple rootstocks.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。