{"title":"番茄根瘤菌 AG1-IA 感染需要宿主和病原体肌醇-1-磷酸合成酶。","authors":"Kriti Tyagi, Ravindra K Chandan, Debashis Sahoo, Srayan Ghosh, Santosh Kumar Gupta, Gopaljee Jha","doi":"10.1111/mpp.13470","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 10","pages":"e13470"},"PeriodicalIF":4.8000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11458890/pdf/","citationCount":"0","resultStr":"{\"title\":\"The host and pathogen myo-inositol-1-phosphate synthases are required for Rhizoctonia solani AG1-IA infection in tomato.\",\"authors\":\"Kriti Tyagi, Ravindra K Chandan, Debashis Sahoo, Srayan Ghosh, Santosh Kumar Gupta, Gopaljee Jha\",\"doi\":\"10.1111/mpp.13470\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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. 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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. 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引用次数: 0
摘要
肌醇-1-磷酸合成酶(MIPS)催化肌醇的生物合成,肌醇是一种重要的糖类,可调节植物的各种生理和生化过程。在这里,我们提供的证据表明,番茄成功感染毁灭性坏死性真菌病原体根瘤菌(Rhizoctonia solani)需要宿主(SlMIPS1)和病原体(Rs_MIPS)肌醇-1-磷酸合成酶(MIPS)基因。Silencing of SlMIPS1 or Rs_MIPS 可以防止病害的发生,而外源喷洒肌醇则会增强病害的严重程度。R.solani感染后,SlMIPS1上调,可能促进了源到汇的转换,诱导了SWEET基因的表达,促进了受感染组织中糖的供应。此外,水杨酸(SA)-茉莉酸平衡被改变,SA 介导的防御被抑制,因此促进了病害的发生。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。病毒诱导的 NPR1(SA 信号转导中的一个关键基因)基因沉默使 SlMIPS1 沉默的番茄品系易受感染。这些分析表明,SA 介导的防御诱导使 SlMIPS1 沉默的番茄品系具有抗病性。此外,我们还提出了 SlMIPS1 和 SA 相互负调控以调节防御反应的证据。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 R. solani 在重要农作物上引起的病害的一个重要策略。
The host and pathogen myo-inositol-1-phosphate synthases are required for Rhizoctonia solani AG1-IA infection in tomato.
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.
期刊介绍:
Molecular Plant Pathology is now an open access journal. Authors pay an article processing charge to publish in the journal and all articles will be freely available to anyone. BSPP members will be granted a 20% discount on article charges. The Editorial focus and policy of the journal has not be changed and the editorial team will continue to apply the same rigorous standards of peer review and acceptance criteria.