Polygalacturonase-Inhibiting Protein Interacts with Pectin through a Binding Site Formed by Four Clustered Residues of Arginine and Lysine

Spadoni, Sara; Zabotina, Olga A.; Matteo, Adele Di; Mikkelsen, Jørn Dalgaard; Cervone, Felice; Lorenzo, Giulia De; Mattei, Benedetta; Bellincampi, Daniela

doi:10.1104/pp.106.076950

Cited by 87 publications

(77 citation statements)

References 43 publications

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“…The observation that the Arabidopsis wall-associated kinase WAK1 (Decreux and Messiaen, 2005), which is able to bind polygalacturonic acid, is induced by bacterial infection and that this induction is required for survival upon treatments with chemical inducers of resistance supports this hypothesis (He et al, 1998). Apoplastic proteins that have domains interacting with pectin also include a peroxidase (Carpin et al, 2001) and PGIP (Spadoni et al, 2006); these proteins may participate to perceive alterations of pectin structure and transmit this information across the plasma membrane with mech-anisms not yet investigated.…”

Section: Discussionmentioning

confidence: 64%

Transgenic Expression of a Fungal endo-Polygalacturonase Increases Plant Resistance to Pathogens and Reduces Auxin Sensitivity

et al. 2007

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Polygalacturonases (PGs), enzymes that hydrolyze the homogalacturonan of the plant cell wall, are virulence factors of several phytopathogenic fungi and bacteria. On the other hand, PGs may activate defense responses by releasing oligogalacturonides (OGs) perceived by the plant cell as host-associated molecular patterns. Tobacco (Nicotiana tabacum) and Arabidopsis (Arabidopsis thaliana) plants expressing a fungal PG (PG plants) have a reduced content of homogalacturonan. Here, we show that PG plants are more resistant to microbial pathogens and have constitutively activated defense responses. Interestingly, either in tobacco PG or wild-type plants treated with OGs, resistance to fungal infection is suppressed by exogenous auxin, whereas sensitivity to auxin of PG plants is reduced in different bioassays. The altered plant defense responses and auxin sensitivity in PG plants may reflect an increased accumulation of OGs and subsequent antagonism of auxin action. Alternatively, it may be a consequence of perturbations of cellular physiology and elevated defense status as a result of altered cell wall architecture.

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Section: Discussionmentioning

confidence: 64%

Transgenic Expression of a Fungal endo-Polygalacturonase Increases Plant Resistance to Pathogens and Reduces Auxin Sensitivity

et al. 2007

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“…It is conceivable that abundance or modification of cell wall polymers is monitored directly; for example, by physical interaction with the extracellular domain of RLP44, perhaps in a way similar to that of the pectin-binding wall-associated kinases (4,5). Although there is as of yet no evidence supporting this hypothesis, it is noteworthy that at least one LRR protein, the polygalacturonase inhibitor protein, can interact with de-methylesterified pectin in the wall (37). Importantly, the abundance of this particular cell wall polymer is affected in the PMEIox line used as genetic background for the suppressor screen, which identified RLP44 (14).…”

Section: Discussionmentioning

confidence: 97%

A receptor-like protein mediates the response to pectin modification by activating brassinosteroid signaling

Wolf

Does

Ladwig

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

160

187

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The brassinosteroid (BR) signaling module is a central regulator of plant morphogenesis, as indicated by the large number of BRresponsive cell wall-related genes and the severe growth defects of BR mutants. Despite a detailed knowledge of the signaling components, the logic of this auto-/paracrine signaling module in growth control remains poorly understood. Recently, extensive cross-talk with other signaling pathways has been shown, suggesting that the outputs of BR signaling, such as gene-expression changes, are subject to complex control mechanisms. We previously provided evidence for a role of BR signaling in a feedback loop controlling the integrity of the cell wall. Here, we identify the first dedicated component of this feedback loop: a receptor-like protein (RLP44), which is essential for the compensatory triggering of BR signaling upon inhibition of pectin de-methylesterification in the cell wall. RLP44 is required for normal growth and stress responses and connects with the BR signaling pathway, presumably through a direct interaction with the regulatory receptor-like kinase BAK1. These findings corroborate a role for BR in controlling the sensitivity of a feedback signaling module involved in maintaining the physicochemical homeostasis of the cell wall during cell expansion.brassinosteroids | cell wall integrity | pectin

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“…However, there are several other possible mechanisms that may contribute to PG and Exp dependent alterations in pathogen susceptibility. For example, alterations in fruit CW structure resulting from reduced PG and Exp abundance may serve to retain inhibitors of pathogen function, such as PGIPs, whose loss of CW association during ripening has been correlated with elevated pathogen susceptibility (37)(38)(39). PG and Exp reduction also may alter pathogen-induced responses, a mechanism suggested by the demonstration that CW changes can activate novel defense pathways (40).…”

Section: Discussionmentioning

confidence: 99%

The intersection between cell wall disassembly, ripening, and fruit susceptibility to Botrytis cinerea

Cantu

Vicente²,

Greve³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

268

209

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Fruit ripening is characterized by processes that modify texture and flavor but also by a dramatic increase in susceptibility to necrotrophic pathogens, such as Botrytis cinerea. Disassembly of the major structural polysaccharides of the cell wall (CW) is a significant process associated with ripening and contributes to fruit softening. In tomato, polygalacturonase (PG) and expansin (Exp) are among the CW proteins that cooperatively participate in ripening-associated CW disassembly. To determine whether endogenous CW disassembly influences the ripening-regulated increase in necrotropic pathogen susceptibility, B. cinerea susceptibility was assessed in transgenic fruit with suppressed polygalacturonase (LePG) and expansin (LeExp1) expression. Suppression of either LePG or LeExp1 alone did not reduce susceptibility but simultaneous suppression of both dramatically reduced the susceptibility of ripening fruit to B. cinerea, as measured by fungal biomass accumulation and by macerating lesion development. These results demonstrate that altering endogenous plant CW disassembly during ripening influences the course of infection by B. cinerea, perhaps by changing the structure or the accessibility of CW substrates to pathogen CW-degrading enzymes. Recognition of the role of ripening-associated CW metabolism in postharvest pathogen susceptibility may be useful in the design and development of strategies to limit pathogen losses during fruit storage, handling, and distribution.expansin ͉ polygalacturonase ͉ tomato ͉ plant pathogen

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Polygalacturonase-Inhibiting Protein Interacts with Pectin through a Binding Site Formed by Four Clustered Residues of Arginine and Lysine

Cited by 87 publications

References 43 publications

Transgenic Expression of a Fungal endo-Polygalacturonase Increases Plant Resistance to Pathogens and Reduces Auxin Sensitivity

Transgenic Expression of a Fungal endo-Polygalacturonase Increases Plant Resistance to Pathogens and Reduces Auxin Sensitivity

A receptor-like protein mediates the response to pectin modification by activating brassinosteroid signaling

The intersection between cell wall disassembly, ripening, and fruit susceptibility to Botrytis cinerea

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