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

机译:苹果根耐药性对茄生抗性的系统分析及防御激活的基础分子规例

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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.
机译:由病原体复合物引起的Apple Replant疾病(ARD)显着影响苹果园的建立。在最近,尚未研究抗原抗性的分子调控。进行系统的表型努力和一系列转录组分析,以发现苹果根部抗性的底部分子机制对ARD病原体复合物中的代表性成员。基因型特异性植物存活率和生物质减少对应于受感染根的坏死进展模式的显微特征。与伴有易感性基因型的迅速的坏死进展相比,分离健康和坏死部分的定义边界可能导致抗性基因型根的延迟坏死膨胀。来自一系列转录组的综合数据集分析产生了抗性和易感苹果根系之间的防御激活基因组转录网络的第一个全景。早期和更强烈的分子防御活化,例如病原体感知和激素信号传导,可以区分苹果根系中的易感性。多种防御途径的延迟和中断激活可能导致阻力响应不足。使用具有限定抗性和敏感表型的苹果砧木种质面板,通过转基因操作来研究选定的候选基因,包括CRISPR / CAS9工具,用于在苹果根部防御期间对P. Ultimum感染的特定作用。具有验证功能的单个苹果基因可以利用调节根抗性响应的函数,用于开发用于准确和有效地将抗性特征融入新的苹果砧座的分子工具。

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