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转录基因组测序揭示了Vmplc1参与调节低温诱导下Valsa Mali的病原性

Xianglong Meng^1,2, Yage Dong¹, Jiangtao Yin³

¹College of Plant Protection, Hebei Agricultural University, Baoding, 071001, Hebei, P.R. China.

|November 19, 2025

概括

冷增强了Valsa mali的病原性,通过激活特定的基因. Vmplc1信号通路对于这种依赖温度的毒性至关重要,它为更好的宿主殖民重新编程了真菌.

科学领域:

植物病理学植物病理学
菌类学菌类学是指菌类学.
分子生物学分子生物学

背景情况:

果瓦尔萨瘤 (AVC),由瓦尔萨马利 (Vm) 引起,导致严重的经济损失.
背后的分子机制冷的Vm病原性还没有很好地理解.

研究的目的:

调查瓦尔萨马利的冷诱导致病性增强的分子机制.
为了确定关键的基因和途径,涉及到Vm的温度依赖的毒性.

主要方法:

低温原料Vm和受感染的果组织的RNA测序 (RNA-seq) 分析.
不同基因表达分析,包括碳水化合物活性酶 (CAZymes).
综合性分析和差异表达基因 (DEGs) 的功能分类.
使用突变菌株对候选基因 (包括Vmplc1) 的功能验证.

主要成果:

RNA-seq在原始化髓和冷原始化感染期间发现了数千个DEG.
碳水化合物活性酶 (CAZymes) 的很大一部分,特别是糖化酸酶 (GHs),在冷原始化过程中被上调.
优先考虑了63个核心的冷反应性毒性基因,包括分泌的GH和短链脱酶 (SDR).
编码热传感蛋白的Vmplc1基因被确定为一个关键的信号枢纽,对冷致病性至关重要.
ΔVmplc1突变体表现出明显减少的病变形成和抑制的毒性因子表达.

结论:

通过协调的转录程序,冷原始化增强了Vm的病原性.
通过Vmplc1介导的信号通路对于在寒冷压力下调节病毒效应因子的升级至关重要.
Vmplc1在Vm的热适应中起到关键的调节作用,在低温下增强宿主殖民.

关键词:

瓦尔萨·马利·马利·马利果瓦尔萨是癌症的一种疾病.糖酸酸酶是什么糖酸酸酶是什么低温诱导的诱导方式对转录组进行分析.

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