Medicarpin confers powdery mildew resistance in Medicago truncatula and activates the salicylic acid signalling pathway

Powdery mildew (PM) caused by the obligate biotrophic fungal pathogen Erysiphe pisi is an economically important disease of legumes. Legumes are rich in isoflavonoids, a class of secondary metabolites whose role in PM resistance is ambiguous. Here we show that the pterocarpan medicarpin accumulates...

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Veröffentlicht in:Molecular plant pathology 2022-07, Vol.23 (7), p.966-983
Hauptverfasser: Gupta, Arunima, Awasthi, Pallavi, Sharma, Neha, Parveen, Sajiya, Vats, Ravi P., Singh, Nirpendra, Kumar, Yashwant, Goel, Atul, Chandran, Divya
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container_end_page 983
container_issue 7
container_start_page 966
container_title Molecular plant pathology
container_volume 23
creator Gupta, Arunima
Awasthi, Pallavi
Sharma, Neha
Parveen, Sajiya
Vats, Ravi P.
Singh, Nirpendra
Kumar, Yashwant
Goel, Atul
Chandran, Divya
description Powdery mildew (PM) caused by the obligate biotrophic fungal pathogen Erysiphe pisi is an economically important disease of legumes. Legumes are rich in isoflavonoids, a class of secondary metabolites whose role in PM resistance is ambiguous. Here we show that the pterocarpan medicarpin accumulates at fungal infection sites, as analysed by fluorescein‐tagged medicarpin, and provides penetration and post‐penetration resistance against E. pisi in Medicago truncatula in part through the activation of the salicylic acid (SA) signalling pathway. Comparative gene expression and metabolite analyses revealed an early induction of isoflavonoid biosynthesis and accumulation of the defence phytohormones SA and jasmonic acid (JA) in the highly resistant M. truncatula genotype A17 but not in moderately susceptible R108 in response to PM infection. Pretreatment of R108 leaves with medicarpin increased SA levels, SA‐associated gene expression, and accumulation of hydrogen peroxide at PM infection sites, and reduced fungal penetration and colony formation. Strong parallels in the levels of medicarpin and SA, but not JA, were observed on medicarpin/SA treatment pre‐ or post‐PM infection. Collectively, our results suggest that medicarpin and SA may act in concert to restrict E. pisi growth, providing new insights into the metabolic and signalling pathways required for PM resistance in legumes. Infection‐localized accumulation of the isoflavonoid phytoalexin medicarpin provides resistance against the pea powdery mildew pathogen and activates salicylic acid signalling in Medicago truncatula.
doi_str_mv 10.1111/mpp.13202
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Legumes are rich in isoflavonoids, a class of secondary metabolites whose role in PM resistance is ambiguous. Here we show that the pterocarpan medicarpin accumulates at fungal infection sites, as analysed by fluorescein‐tagged medicarpin, and provides penetration and post‐penetration resistance against E. pisi in Medicago truncatula in part through the activation of the salicylic acid (SA) signalling pathway. Comparative gene expression and metabolite analyses revealed an early induction of isoflavonoid biosynthesis and accumulation of the defence phytohormones SA and jasmonic acid (JA) in the highly resistant M. truncatula genotype A17 but not in moderately susceptible R108 in response to PM infection. Pretreatment of R108 leaves with medicarpin increased SA levels, SA‐associated gene expression, and accumulation of hydrogen peroxide at PM infection sites, and reduced fungal penetration and colony formation. Strong parallels in the levels of medicarpin and SA, but not JA, were observed on medicarpin/SA treatment pre‐ or post‐PM infection. Collectively, our results suggest that medicarpin and SA may act in concert to restrict E. pisi growth, providing new insights into the metabolic and signalling pathways required for PM resistance in legumes. 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Legumes are rich in isoflavonoids, a class of secondary metabolites whose role in PM resistance is ambiguous. Here we show that the pterocarpan medicarpin accumulates at fungal infection sites, as analysed by fluorescein‐tagged medicarpin, and provides penetration and post‐penetration resistance against E. pisi in Medicago truncatula in part through the activation of the salicylic acid (SA) signalling pathway. Comparative gene expression and metabolite analyses revealed an early induction of isoflavonoid biosynthesis and accumulation of the defence phytohormones SA and jasmonic acid (JA) in the highly resistant M. truncatula genotype A17 but not in moderately susceptible R108 in response to PM infection. Pretreatment of R108 leaves with medicarpin increased SA levels, SA‐associated gene expression, and accumulation of hydrogen peroxide at PM infection sites, and reduced fungal penetration and colony formation. Strong parallels in the levels of medicarpin and SA, but not JA, were observed on medicarpin/SA treatment pre‐ or post‐PM infection. Collectively, our results suggest that medicarpin and SA may act in concert to restrict E. pisi growth, providing new insights into the metabolic and signalling pathways required for PM resistance in legumes. Infection‐localized accumulation of the isoflavonoid phytoalexin medicarpin provides resistance against the pea powdery mildew pathogen and activates salicylic acid signalling in Medicago truncatula.</abstract><cop>England</cop><pub>John Wiley &amp; Sons, Inc</pub><pmid>35263504</pmid><doi>10.1111/mpp.13202</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0003-2758-2461</orcidid><orcidid>https://orcid.org/0000-0001-6206-8826</orcidid><oa>free_for_read</oa></addata></record>
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subjects Accumulation
Airborne microorganisms
Alfalfa
Biosynthesis
Economic importance
Flavonoids
Fluorescein
fluorescein‐tagged medicarpin
Fungi
Gene expression
Genomes
Genotypes
Hydrogen peroxide
Infections
isoflavone reductase
Isoflavonoids
Jasmonic acid
Legumes
Medicago truncatula
Metabolites
Original
Pathogens
Penetration
Penetration resistance
phytoalexin
Plant diseases
Plant hormones
Powdery mildew
Salicylic acid
Secondary metabolites
Signal transduction
Signaling
title Medicarpin confers powdery mildew resistance in Medicago truncatula and activates the salicylic acid signalling pathway
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