VmAGP1劫持了一种植物激酶-ATPase级联,以驱动自我破坏性宿主酸化
Yinghao Wang1, Keqian Yao1, Mengjie Gao1
1State Key Laboratory for Crop Stress Resistance and High-Efficiency Production, College of Plant Protection, Northwest A&F University, Yangling, 712100, China.
Journal of integrative plant biology
|November 17, 2025
概括
瓦尔萨马利分泌VmAGP1来操纵果细胞的pH值,促进感染. 这种真菌毒性因子触发了一条涉及MdLecRK2和MdVHAc"1的途径,降低细胞内pH值,帮助疾病发展.
科学领域:
- 植物病理学 植物病理学
- 分子植物-微生物相互作用
- 生物化学 生物化学
背景情况:
- 像Valsa mali这样的真菌病原体会使宿主环境酸化,以增强感染力.
- 在感染期间,V. mali用于pH调节的精确细胞机制尚未完全理解.
研究的目的:
- 阐明Valsa mali操纵宿主细胞pH值以促进感染的分子机制.
- 为了确定关键的毒性因素和参与V. mali病变的宿主目标.
主要方法:
- 酵母两杂交 (Y2H),双分子光补充 (BiFC) 和共免疫沉 (Co-IP) 试验用于研究蛋白质相互作用.
- 露西法酶补充成像 (LCI) 来确认蛋白质二分化.
- 流细胞计测量以评估果原生质中的细胞内pH值变化.
主要成果:
- 一种V. mali毒性因子VmAGP1与果受体类激酶MdLecRK2相互作用,从而对疾病耐药性产生负面调节.
- VmAGP1促进MdLecRK2的同位二分化,导致真空H+-ATPaseMdVHAc"1.1"的相互作用和酸化.
- VmAGP1的表达会使果原生质酸化,这种过程由MdLecRK2/MdVHAc"1的过度表达加剧.
结论:
- 瓦尔萨马利利用VmAGP1诱导MdLecRK2的同位二分化,并与MdVHAc"1.1"启动酸化级联.
- 这一连串的结果是果细胞的酸化,促进了V. mali感染.
- 这项研究揭示了V. mali病变的新型pH操纵策略,并确定了控制果瓦尔萨癌症的潜在目标.
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