Spore Density Determines Infection Strategy by the Plant Pathogenic Fungus <i>Plectosphaerella cucumerina</i>

Pétriacq, Pierre; Stassen, Joost H. M.; Ton, Jurriaan

doi:10.1104/pp.15.00551

Cited by 59 publications

(50 citation statements)

References 100 publications

(170 reference statements)

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“…Differences in class distributions between genotype–treatment combinations were analysed for statistical significance, using Fisher's exact tests (R, v.3.1.2). To ensure necrotrophic infection, assays with Pc (strain BMM) were based on droplet inoculation (6 μl, 5 × 10 6 spores ml −1 ) on four to six fully expanded leaves of eight plants at the 18‐leaf stage (4.5 wk old at a CO 2 ), as described previously (Pétriacq et al ., ). Disease progression was measured as lesion diameters at 13 dpi.…”

Section: Methodsmentioning

confidence: 97%

Mechanisms of glacial‐to‐future atmospheric CO₂ effects on plant immunity

et al. 2018

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Summary The impacts of rising atmospheric CO2 concentrations on plant disease have received increasing attention, but with little consensus emerging on the direct mechanisms by which CO2 shapes plant immunity. Furthermore, the impact of sub‐ambient CO 2 concentrations, which plants have experienced repeatedly over the past 800 000 yr, has been largely overlooked.A combination of gene expression analysis, phenotypic characterisation of mutants and mass spectrometry‐based metabolic profiling was used to determine development‐independent effects of sub‐ambient CO 2 (sa CO 2) and elevated CO 2 (eCO 2) on Arabidopsis immunity.Resistance to the necrotrophic Plectosphaerella cucumerina (Pc) was repressed at sa CO 2 and enhanced at eCO 2. This CO 2‐dependent resistance was associated with priming of jasmonic acid (JA)‐dependent gene expression and required intact JA biosynthesis and signalling. Resistance to the biotrophic oomycete Hyaloperonospora arabidopsidis (Hpa) increased at both eCO 2 and sa CO 2. Although eCO 2 primed salicylic acid (SA)‐dependent gene expression, mutations affecting SA signalling only partially suppressed Hpa resistance at eCO 2, suggesting additional mechanisms are involved. Induced production of intracellular reactive oxygen species (ROS) at sa CO 2 corresponded to a loss of resistance in glycolate oxidase mutants and increased transcription of the peroxisomal catalase gene CAT2, unveiling a mechanism by which photorespiration‐derived ROS determined Hpa resistance at saCO2.By separating indirect developmental impacts from direct immunological effects, we uncover distinct mechanisms by which CO 2 shapes plant immunity and discuss their evolutionary significance.

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Section: Methodsmentioning

confidence: 97%

Mechanisms of glacial‐to‐future atmospheric CO₂ effects on plant immunity

et al. 2018

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“…Cell death was assessed by conductivity measurements of electrolyte leakage from four biological replicates (n = 4) as reported (Pétriacq et al, 2016). Briefly, 5-week-old plants were syringe infiltrated with 10 mM MgCl 2 or Pst-AvrRpm1 (10 5 colony-forming units mL 21 ), and 48 hpi, six discs (total area of 1.2 cm 2 ) from leaves of the same developmental age were punched on different plants using a cork borer and floated onto 2 mL of double-deionized sterile water in 2-mL tubes.…”

Section: Cell Death Measurementsmentioning

confidence: 99%

“…Callose deposition was measured from 5-week-old leaves stained with Aniline Blue using a UV epifluorescence microscope (Olympus BX51) as described previously (Pétriacq et al, 2016). For each condition, 12 leaves from different plants (n = 12) were analyzed in Photoshop CS4 (Adobe), and callose intensity was expressed as relative callose area as described previously (Pétriacq et al, 2016).…”

Section: Quantification Of Callose Depositionmentioning

confidence: 99%

“…Briefly, four leaves from 5-week-old plants were pooled (n = 3), flash frozen in liquid nitrogen 20 h after infection with Pst-AvrRpm1 or 24 h after syringe infiltration with water or NAD + (1 mM), and then stored at 280°C until RNA extraction and RT-qPCR analyses. mRNA abundances were expressed relative to the ACTIN2 reference gene (At3g18780) using previously described gene-specific primers (Oelze et al, 2012;Pétriacq et al, 2012;Gouhier-Darimont et al, 2013;Gruner et al, 2013;Pétriacq et al, 2016). The sequences of RT-qPCR primers are given in Supplemental Table S4.…”

Section: Transcript Abundancementioning

confidence: 99%

“…For each condition, 12 leaves from different plants (n = 12) were analyzed in Photoshop CS4 (Adobe), and callose intensity was expressed as relative callose area as described previously (Pétriacq et al, 2016).…”

Section: Quantification Of Callose Depositionmentioning

confidence: 99%

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NAD Acts as an Integral Regulator of Multiple Defense Layers

et al. 2016

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(J.T.).Pyridine nucleotides, such as NAD, are crucial redox carriers and have emerged as important signaling molecules in stress responses. Previously, we have demonstrated in Arabidopsis (Arabidopsis thaliana) that the inducible NAD-overproducing nadC lines are more resistant to an avirulent strain of Pseudomonas syringae pv tomato (Pst-AvrRpm1), which was associated with salicylic acid-dependent defense. Here, we have further characterized the NAD-dependent immune response in Arabidopsis. Quinolinate-induced stimulation of intracellular NAD in transgenic nadC plants enhanced resistance against a diverse range of (a)virulent pathogens, including Pst-AvrRpt2, Dickeya dadantii, and Botrytis cinerea. Characterization of the redox status demonstrated that elevated NAD levels induce reactive oxygen species (ROS) production and the expression of redox marker genes of the cytosol and mitochondrion. Using pharmacological and reverse genetics approaches, we show that NAD-induced ROS production functions independently of NADPH oxidase activity and light metabolism but depends on mitochondrial respiration, which was increased at higher NAD. We further demonstrate that NAD primes pathogen-induced callose deposition and cell death. Mass spectrometry analysis reveals that NAD simultaneously induces different defense hormones and that the NAD-induced metabolic profiles are similar to those of defense-expressing plants after treatment with pathogen-associated molecular patterns. We thus conclude that NAD triggers metabolic profiles rather similar to that of pathogen-associated molecular patterns and discuss how signaling cross talk between defense hormones, ROS, and NAD explains the observed resistance to pathogens.

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