Plant-Microbe Interactions Laboratory, National Institute of Plant Genome Research, New Delhi, India.
Mol Plant Pathol. 2024 Oct;25(10):e13470. doi: 10.1111/mpp.13470.
The myo-inositol-1-phosphate synthase (MIPS) catalyses the biosynthesis of myo-inositol, an important sugar that regulates various physiological and biochemical processes in plants. Here, we provide evidence that host (SlMIPS1) and pathogen (Rs_MIPS) myo-inositol-1-phosphate synthase (MIPS) genes are required for successful infection of Rhizoctonia solani, a devastating necrotrophic fungal pathogen, in tomato. Silencing of either SlMIPS1 or Rs_MIPS prevented disease, whereas an exogenous spray of myo-inositol enhanced disease severity. SlMIPS1 was upregulated upon R. solani infection, and potentially promoted source-to-sink transition, induced SWEET gene expression, and facilitated sugar availability in the infected tissues. In addition, salicylic acid (SA)-jasmonic acid homeostasis was altered and SA-mediated defence was suppressed; therefore, disease was promoted. On the other hand, silencing of SlMIPS1 limited sugar availability and induced SA-mediated defence to prevent R. solani infection. Virus-induced gene silencing of NPR1, a key gene in SA signalling, rendered SlMIPS1-silenced tomato lines susceptible to infection. These analyses suggest that induction of SA-mediated defence imparts disease tolerance in SlMIPS1-silenced tomato lines. In addition, we present evidence that SlMIPS1 and SA negatively regulate each other to modulate the defence response. SA treatment reduced SlMIPS1 expression and myo-inositol content in tomato, whereas myo-inositol treatment prevented SA-mediated defence. We emphasize that downregulation of host/pathogen MIPS can be an important strategy for controlling diseases caused by R. solani in agriculturally important crops.
肌醇-1-磷酸合酶 (MIPS) 催化肌醇的生物合成，肌醇是一种重要的糖，调节植物中的各种生理和生化过程。在这里，我们提供证据表明，宿主（SlMIPS1）和病原体（Rs_MIPS）肌醇-1-磷酸合酶（MIPS）基因对于番茄中毁灭性的坏死真菌病原体立枯丝核菌的成功感染是必需的。沉默 SlMIPS1 或 Rs_MIPS 都能阻止疾病，而外源喷洒肌醇则会加剧疾病的严重程度。SlMIPS1 在 R. solani 感染后上调，并可能促进源到汇的转变，诱导 SWEET 基因表达，并促进感染组织中糖的可用性。此外，水杨酸 (SA)-茉莉酸稳态被改变，SA 介导的防御被抑制；因此，疾病得到了促进。另一方面，沉默 SlMIPS1 限制了糖的可用性，并诱导 SA 介导的防御以防止 R. solani 感染。水杨酸信号关键基因 NPR1 的病毒诱导基因沉默使 SlMIPS1 沉默的番茄品系易受感染。这些分析表明，诱导 SA 介导的防御赋予 SlMIPS1 沉默的番茄品系疾病耐受性。此外，我们提供的证据表明，SlMIPS1 和 SA 相互负调控以调节防御反应。SA 处理降低了番茄中 SlMIPS1 的表达和肌醇含量，而肌醇处理则阻止了 SA 介导的防御。我们强调，下调宿主/病原体 MIPS 可能是控制农业上重要作物中由 R. solani 引起的疾病的重要策略。
