Zhu Yanmin, Saltzgiver Melody
USDA-ARS, Tree Fruit Research Laboratory, Wenatchee, WA 98801 USA.
Hortic Res. 2020 May 1;7(1):62. doi: 10.1038/s41438-020-0286-4. eCollection 2020.
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 , 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 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.
苹果再植病（ARD）由一种病原菌复合体引起，对苹果园的建立有重大影响。直到最近才开始研究ARD抗性的分子调控机制。我们进行了系统的表型分析和一系列转录组分析，以揭示苹果根系对ARD病原菌复合体中代表性成员——[病原菌名称未给出]的抗性潜在分子机制。基因型特异性的植株存活率和生物量减少与感染根上坏死进展模式的微观特征相对应。与感病基因型感染根上坏死迅速进展和大量菌丝生长相比，抗性基因型根中健康和坏死部分之间存在明确界限可能导致坏死扩展延迟。一系列转录组分析生成的综合数据集首次全景展示了抗性和感病苹果根系全基因组防御激活转录网络。早期更强的分子防御激活，如病原菌感知和激素信号传导，可能是苹果根系抗性与感病性的区别所在。多种防御途径的延迟和中断激活可能导致抗性反应不足。利用具有明确抗性和感病表型的苹果砧木种质库，正在通过转基因操作（包括CRISPR/Cas9工具）研究选定候选基因在苹果根系抵御[病原菌名称未给出]感染过程中的特定作用。具有调控根系抗性反应功能验证的单个苹果基因可用于开发分子工具，以便准确高效地将抗性性状整合到新的苹果砧木中。
