Necrotizing activity of five <i>Botrytis cinerea</i> endopolygalacturonases produced in <i>Pichia pastoris</i>

Kars, I.; Krooshof, Geja H.; Wagemakers, L.; Joosten, R.; Benen, J.A.E.; Kan, Jan A.L. van

doi:10.1111/j.1365-313x.2005.02436.x

Cited by 249 publications

(244 citation statements)

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“…The most extensively studied PGs from fungal plant pathogens are those of Botrytis cinerea (for review, see Zhang and van Kan, 2013b), a necrotrophic broad-host-range pathogen that contains six PG genes (designated Bcpg1-Bcpg6) in its genome (Wubben et al, 1999). Deletion of either Bcpg1 or Bcpg2 resulted in a strong reduction in virulence on tomato and broad bean (Vicia faba) leaves (ten Have et al, 1998;Kars et al, 2005), presumably because the enzymes have a detrimental effect on the integrity of host cell walls and tissues. Indeed, infiltrating BcPG2 into broad bean leaves or transient expression of BcPG2 in Nicotiana benthamiana led to tissue collapse and necrosis, and the necrotic response was abolished when the catalytic domain of the PG was mutated (Kars et al, 2005;Joubert et al, 2007).…”

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Fungal Endopolygalacturonases Are Recognized as Microbe-Associated Molecular Patterns by the Arabidopsis Receptor-Like Protein RESPONSIVENESS TO BOTRYTIS POLYGALACTURONASES1

et al. 2013

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Plants perceive microbial invaders using pattern recognition receptors that recognize microbe-associated molecular patterns. In this study, we identified RESPONSIVENESS TO BOTRYTIS POLYGALACTURONASES1 (RBPG1), an Arabidopsis (Arabidopsis thaliana) leucine-rich repeat receptor-like protein, AtRLP42, that recognizes fungal endopolygalacturonases (PGs) and acts as a novel microbe-associated molecular pattern receptor. RBPG1 recognizes several PGs from the plant pathogen Botrytis cinerea as well as one from the saprotroph Aspergillus niger. Infiltration of B. cinerea PGs into Arabidopsis accession Columbia induced a necrotic response, whereas accession Brno (Br-0) showed no symptoms. A map-based cloning strategy, combined with comparative and functional genomics, led to the identification of the Columbia RBPG1 gene and showed that this gene is essential for the responsiveness of Arabidopsis to the PGs. Transformation of RBPG1 into accession Br-0 resulted in a gain of PG responsiveness. Transgenic Br-0 plants expressing RBPG1 were equally susceptible as the recipient Br-0 to the necrotroph B. cinerea and to the biotroph Hyaloperonospora arabidopsidis. Pretreating leaves of the transgenic plants with a PG resulted in increased resistance to H. arabidopsidis. Coimmunoprecipitation experiments demonstrated that RBPG1 and PG form a complex in Nicotiana benthamiana, which also involves the Arabidopsis leucine-rich repeat receptor-like protein SOBIR1 (for SUPPRESSOR OF BIR1). sobir1 mutant plants did not induce necrosis in response to PGs and were compromised in PG-induced resistance to H. arabidopsidis.

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Fungal Endopolygalacturonases Are Recognized as Microbe-Associated Molecular Patterns by the Arabidopsis Receptor-Like Protein RESPONSIVENESS TO BOTRYTIS POLYGALACTURONASES1

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“…Moreover, the B. cinerea endopolygalacturonases Bcpg1 and Bcpg2 and the PME Bcpme1 are required for full virulence (ten Have et al, 1998;Valette-Collet et al, 2003;Kars et al, 2005), illustrating the importance of pectin degradation for the success of this pathogen.…”

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Arabidopsis PECTIN METHYLESTERASEs Contribute to Immunity against Pseudomonas syringae

et al. 2013

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Pectins, major components of dicot cell walls, are synthesized in a heavily methylesterified form in the Golgi and are partially deesterified by pectin methylesterases (PMEs) upon export to the cell wall. PME activity is important for the virulence of the necrotrophic fungal pathogen Botrytis cinerea. Here, the roles of Arabidopsis PMEs in pattern-triggered immunity and immune responses to the necrotrophic fungus Alternaria brassicicola and the bacterial hemibiotroph Pseudomonas syringae pv maculicola ES4326 (Pma ES4326) were studied. Plant PME activity increased during pattern-triggered immunity and after inoculation with either pathogen. The increase of PME activity in response to pathogen treatment was concomitant with a decrease in pectin methylesterification. The pathogen-induced PME activity did not require salicylic acid or ethylene signaling, but was dependent on jasmonic acid signaling. In the case of induction by A. brassicicola, the ethylene response factor, but not the MYC2 branch of jasmonic acid signaling, contributed to induction of PME activity, whereas in the case of induction by Pma ES4326, both branches contributed. There are 66 PME genes in Arabidopsis, suggesting extensive genetic redundancy. Nevertheless, selected pme single, double, triple and quadruple mutants allowed significantly more growth of Pma ES4326 than wild-type plants, indicating a role of PMEs in resistance to this pathogen. No decreases in total PME activity were detected in these pme mutants, suggesting that the determinant of immunity is not total PME activity; rather, it is some specific effect of PMEs such as changes in the pattern of pectin methylesterification.The plant cell wall determines cell shape, facilitates cell-cell interaction, and provides mechanical strength to plant cells. De Bary (1886) first observed that a plant pathogen, Sclerotina sclerotiorum, degraded host cell walls during infection. Later, it was concluded that plant cell walls act as preformed structural barriers against pathogen entry, because it was noticed that many plant pathogens produced various types of cell wall-degrading enzymes and that some of those were required for optimal infection of host plants (Albersheim et al., 1969).Arabidopsis mesophyll cells are surrounded by primary cell walls consisting of three major components: cellulose, hemicelluloses, and pectins. Pectins make up approximately 50% of Arabidopsis leaf cell walls (Zablackis et al., 1995;Harholt et al., 2010). They are complex GalA-containing polysaccharides composed of homogalacturonan (HG), rhamnogalacturonan I and II, and xylogalacturonan (Mohnen, 2008). HG is typically the most abundant polysaccharide, constituting approximately 65% of the pectin (Mohnen, 2008;Harholt et al., 2010). HG is a linear homopolymer of 1,4-linked GalA and is synthesized in the Golgi in a highly methylesterified form (Caffall and Mohnen, 2009). Pectin methylesterases (PMEs) demethylesterify HG in the apoplast (Mohnen, 2008;Harholt et al., 2010). Demethylesterification of pectin is considered t...

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“…During B. cinerea infections of plant tissues, cell wall-degrading enzymes are secreted by the fungus. Although some of these enzymes are required for virulence (ten Have et al, , 2001Kars et al, 2005), the fungus fails to infect ripe fruit in the absence of endogenous fruit cell wall disassembly (Cantu et al, 2008a).…”

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Ripening-Regulated Susceptibility of Tomato Fruit toBotrytis cinereaRequiresNORBut NotRINor Ethylene

Cantu

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et al. 2009

Plant Physiology

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Fruit ripening is a developmental process that is associated with increased susceptibility to the necrotrophic pathogen Botrytis cinerea. Histochemical observations demonstrate that unripe tomato (Solanum lycopersicum) fruit activate pathogen defense responses, but these responses are attenuated in ripe fruit infected by B. cinerea. Tomato fruit ripening is regulated independently and cooperatively by ethylene and transcription factors, including NON-RIPENING (NOR) and RIPENING-INHIBITOR (RIN). Mutations in NOR or RIN or interference with ethylene perception prevent fruit from ripening and, thereby, would be expected to influence susceptibility. We show, however, that the susceptibility of ripe fruit is dependent on NOR but not on RIN and only partially on ethylene perception, leading to the conclusion that not all of the pathways and events that constitute ripening render fruit susceptible. Additionally, on unripe fruit, B. cinerea induces the expression of genes also expressed as uninfected fruit ripen. Among the ripening-associated genes induced by B. cinerea are LePG (for polygalacturonase) and LeExp1 (for expansin), which encode cell wall-modifying proteins and have been shown to facilitate susceptibility. LePG and LeExp1 are induced only in susceptible rin fruit and not in resistant nor fruit. Thus, to infect fruit, B. cinerea relies on some of the processes and events that occur during ripening, and the fungus induces these pathways in unripe fruit, suggesting that the pathogen itself can initiate the induction of susceptibility by exploiting endogenous developmental programs. These results demonstrate the developmental plasticity of plant responses to the fungus and indicate how known regulators of fruit ripening participate in regulating ripening-associated pathogen susceptibility.

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Necrotizing activity of five Botrytis cinerea endopolygalacturonases produced in Pichia pastoris

Cited by 249 publications

References 51 publications

Fungal Endopolygalacturonases Are Recognized as Microbe-Associated Molecular Patterns by the Arabidopsis Receptor-Like Protein RESPONSIVENESS TO BOTRYTIS POLYGALACTURONASES1

Fungal Endopolygalacturonases Are Recognized as Microbe-Associated Molecular Patterns by the Arabidopsis Receptor-Like Protein RESPONSIVENESS TO BOTRYTIS POLYGALACTURONASES1

Arabidopsis PECTIN METHYLESTERASEs Contribute to Immunity against Pseudomonas syringae

Ripening-Regulated Susceptibility of Tomato Fruit toBotrytis cinereaRequiresNORBut NotRINor Ethylene

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