Evidence map›Paper›PMID 39376048›Full record

ArticleMolecular plant pathology2024

The host and pathogen myo-inositol-1-phosphate synthases are required for Rhizoctonia solani AG1-IA infection in tomato.

Kriti Tyagi, Ravindra K Chandan, Debashis Sahoo, Srayan Ghosh, Santosh Kumar Gupta, Gopaljee Jha

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In one paragraph

Article in Molecular plant pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Kriti TyagiPlant-Microbe Interactions Laboratory, National Institute of Plant Genome Research, New Delhi, India.
Ravindra K ChandanPlant-Microbe Interactions Laboratory, National Institute of Plant Genome Research, New Delhi, India.
Debashis SahooPlant-Microbe Interactions Laboratory, National Institute of Plant Genome Research, New Delhi, India.
Srayan GhoshPlant-Microbe Interactions Laboratory, National Institute of Plant Genome Research, New Delhi, India.
Santosh Kumar GuptaPlant-Microbe Interactions Laboratory, National Institute of Plant Genome Research, New Delhi, India.
Gopaljee JhaPlant-Microbe Interactions Laboratory, National Institute of Plant Genome Research, New Delhi, India.ORCID 0000-0002-3965-3135

Funding

Department of Biotechnology, Ministry of Science and Technology, India 102/IFD/SAN/763/2019-20
6 · The paper itself

Abstract

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.

Indexed as

Myo-Inositol-1-Phosphate SynthasePlant DiseasesRhizoctoniaSolanum lycopersicumCyclopentanesGene Expression Regulation, PlantGene SilencingHost-Pathogen InteractionsInositolOxylipinsPlant ProteinsSalicylic AcidCyclopentanesInositoljasmonic acidMyo-Inositol-1-Phosphate SynthaseOxylipinsPlant ProteinsSalicylic AcidnecrotrophsphytohormonesSA‐mediated defencesheath blight diseasesugar signallingsusceptibility genes

Identifiers

PMID39376048
PMCPMC11458890

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.