<i>Fusarium solani</i>DNase Is a Signal for Increasing Expression of Nonhost Disease Resistance Response Genes, Hypersensitivity, and Pisatin Production

Hadwiger, Lee A.; Chang, Ming‐Mei; Parsons, M. Angela

doi:10.1094/mpmi-8-0871

Cited by 33 publications

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“…Further analysis of the root exudates suggested that pisatin was at least partly responsible for the inhibition of Fop germination observed in the root exudates of JI 2480. Pisatin is the main pea phytoalexin induced in response to pathogens and a potent antifungal metabolite (Cruickshank, ; Christenson & Hadwiger, ; Van Etten, ; Pueppke & Van Etten, ; Hadwiger et al ., ). Here, pisatin was identified as the principal component of the inhibiting fractions of Messire root exudates.…”

Section: Discussionmentioning

confidence: 97%

“…Despite the known function of pisatin in the inducible defence of pea (Hadwiger et al ., ), three sets of evidence suggest that the inhibiting pisatin in root exudates was constitutively secreted by pea roots. First, very low amounts of pisatin, varying from 0.1 to 2.85 μg pisatin mL −1 of root exudates (equivalent to 1.5–53.25 μg per root) were detected within root exudates in the experimental set‐up.…”

Section: Discussionmentioning

confidence: 99%

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Pisatin involvement in the variation of inhibition of Fusarium oxysporum f. sp. pisi spore germination by root exudates of Pisum spp. germplasm

Bani

Cimmino²,

Evidente³

et al. 2018

Plant Pathology

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Fusarium wilt caused by Fusarium oxysporum f. sp. pisi (Fop) is one of the major constraints of pea worldwide. Its control is difficult and is mainly based on the use of resistant cultivars. This study aimed to identify and characterize resistance mechanisms interfering with Fop spore germination, as an additional pre‐penetration resistance mechanism little explored so far. For this, root exudates were collected from 12 pea accessions with differential responses to the disease, from resistant to susceptible, and their effects on Fop germination and growth were determined. While root exudates from most accessions stimulated Fop germination, the root exudates of three accessions, JI 1412, JI 2480 and P42, did not stimulate, or even inhibited, Fop germination. Although some additional compounds might be involved, the analysis showed that the most active metabolite was the pea phytoalexin pisatin. Pisatin was identified in the active fraction of pea root exudate extracts and its amount in the root exudates was negatively correlated with the extent of Fop germination. This suggests an important role of pisatin in the constitutive defence of pea against F. oxysporum.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Pisatin involvement in the variation of inhibition of Fusarium oxysporum f. sp. pisi spore germination by root exudates of Pisum spp. germplasm

Bani

Cimmino²,

Evidente³

et al. 2018

Plant Pathology

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“…Within the first 2 h following inoculation with Fsph, pea DNA damage is detectable and the induction of pea PR genes commences (Hadwiger et al, 1995). Some of the early proteins translated have known functions that may relate to their potential to slow fungal growth and are described as follows:…”

Section: Early Release Of Biotic Signals Following Fungal Contact Witmentioning

confidence: 99%

Anatomy of a nonhost disease resistance response of pea to Fusarium solani: PR gene elicitation via DNase, chitosan and chromatin alterations

Hadwiger

2015

Front. Plant Sci.

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Of the multiplicity of plant pathogens in nature, only a few are virulent on a given plant species. Conversely, plants develop a rapid “nonhost” resistance response to the majority of the pathogens. The anatomy of the nonhost resistance of pea endocarp tissue against a pathogen of bean, Fusarium solani f.sp. phaseoli (Fsph) and the susceptibility of pea to F. solani f sp. pisi (Fspi) has been described cytologically, biochemically and molecular-biologically. Cytological changes have been followed by electron microscope and stain differentiation under white and UV light. The induction of changes in transcription, protein synthesis, expression of pathogenesis-related (PR) genes, and increases in metabolic pathways culminating in low molecular weight, antifungal compounds are described biochemically. Molecular changes initiated by fungal signals to host organelles, primarily to chromatin within host nuclei, are identified according to source of the signal and the mechanisms utilized in activating defense genes. The functions of some PR genes are defined. A hypothesis based on this data is developed to explain both why fungal growth is suppressed in nonhost resistance and why growth can continue in a susceptible reaction.

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“…Chitosan, a β‐1,4‐D‐glucosamine polymer, a natural component of the cell wall of several fungi (Bartnicki‐Garcia, 1970), has been previously used to mimic pathogen attack. It has been shown to promote jasmonate synthesis (Doares et al ., 1995), enhancement of cell wall lignification and phytoalexin production, as well as to induce salicylic acid and PR proteins (Kauss, 1985; Doares et al ., 1995; Hadwiger et al ., 1995; Mason & Davis, 1997). It is already known that chitosan elicits the activation of the membrane‐located β‐1,3‐glucan synthase via an increased influx of Ca 2+ ions with the consequent localized callose deposition on the cell wall surface (Kauss et al ., 1989; Hadwiger, 1999).…”

Section: Introductionmentioning

confidence: 99%

Chitosan induces Ca²⁺‐mediated programmed cell death in soybean cells

et al. 2003

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Summary• Chitosan, a component of the cell wall of many fungi, has been widely used to mimic pathogen attack and has been shown to induce several defence responses.• Here we show that low concentrations (50 µg ml − 1 ) of chitosan are able to induce an increase in cytosolic Ca 2+ concentration ([Ca 2+ ] cyt ), accumulation of H 2 O 2 in the culture medium, induction of the defence gene chalcone synthase ( chs ), and cell death in soybean cells ( Glycine max ).• Chitosan-induced cell death occurred through cytoplasmic shrinkage, chromatin condensation and activation of caspase 3-like protease, suggesting the activation of a programmed cell death (PCD) pathway. Buffering extracellular Ca 2+ with the Ca 2+ chelator EGTA prevents [Ca 2+ ] cyt elevation, H 2 O 2 production and all downstream PCD features, but not cell death.• Higher doses (200 µg ml − 1 ) of chitosan evoked neither Ca 2+ transient and H 2 O 2 production nor caspase 3-like activation, but caused cell death, possibly as a result of plasma membrane disturbance.

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Fusarium solaniDNase Is a Signal for Increasing Expression of Nonhost Disease Resistance Response Genes, Hypersensitivity, and Pisatin Production

Cited by 33 publications

References 0 publications

Pisatin involvement in the variation of inhibition of Fusarium oxysporum f. sp. pisi spore germination by root exudates of Pisum spp. germplasm

Pisatin involvement in the variation of inhibition of Fusarium oxysporum f. sp. pisi spore germination by root exudates of Pisum spp. germplasm

Anatomy of a nonhost disease resistance response of pea to Fusarium solani: PR gene elicitation via DNase, chitosan and chromatin alterations

Chitosan induces Ca²⁺‐mediated programmed cell death in soybean cells

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Fusarium solaniDNase Is a Signal for Increasing Expression of Nonhost Disease Resistance Response Genes, Hypersensitivity, and Pisatin Production

Cited by 33 publications

References 0 publications

Pisatin involvement in the variation of inhibition of Fusarium oxysporum f. sp. pisi spore germination by root exudates of Pisum spp. germplasm

Pisatin involvement in the variation of inhibition of Fusarium oxysporum f. sp. pisi spore germination by root exudates of Pisum spp. germplasm

Anatomy of a nonhost disease resistance response of pea to Fusarium solani: PR gene elicitation via DNase, chitosan and chromatin alterations

Chitosan induces Ca2+‐mediated programmed cell death in soybean cells

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Chitosan induces Ca²⁺‐mediated programmed cell death in soybean cells