Polygalacturonase-inhibiting protein 2 of Phaseolus vulgaris inhibits BcPG1, a polygalacturonase of Botrytis cinerea important for pathogenicity, and protects transgenic plants from infection

Manfredini, Cinzia; Sicilia, Francesca; Ferrari, Simone; Pontiggia, Daniela; Salvi, G.; Caprari, Claudio; Lorito, Matteo; Lorenzo, Giulia De

doi:10.1016/j.pmpp.2005.10.002

Cited by 78 publications

(70 citation statements)

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“…The effectiveness of PGIP genes in controlling diseases has been demonstrated in a wide variety of organisms, such as fungi, bacteria, and even insects (Kalunke et al, 2015). PvPGIP2 is the most effective inhibitor of PGs (D'Ovidio et al, 2004a;Manfredini et al, 2005). This gene exhibited the highest relative expression level after inoculation in the present study.…”

Section: Discussionsupporting

confidence: 51%

“…Oliveira et al (2010) also reported high PvPGIP2 expression in the Pérola bean cultivar, but only at 2 DAI, and there was a decrease in its expression from 3 DAI. Transgenic plants that express PvPGIP2 exhibit a reduction of about 35% in symptoms caused by Botrytis cinerea (Manfredini et al, 2005), and they exhibit reduced symptoms of Rhizoctonia solani, Phytophthora parasitica var. nicotianae, and Peronospora hyoscyami f. sp tabacina attack (Borras-Hidalgo et al, 2012), suggesting that this gene plays a key role in plant innate immunity and contributes to basal resistance against different fungal species.…”

Section: Discussionmentioning

confidence: 99%

“…Genomic analyses have shown that PGIP genes may exist as a single gene, for example in diploid wheat species (Di Giovanni et al, 2008), or are organized into gene families whose members are tandemarranged and may vary from two, as in Arabidopsis thaliana (Ferrari et al, 2003), to 16, as in Brassica napus (Hegedus et al, 2008). The overexpression of PGIP genes in transgenic plants such as wheat, tomato, tobacco, and A. thaliana limits fungal colonization (Powell et al, 2000;Ferrari et al, 2003;Manfredini et al, 2005;Janni et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

“…In the soybean (Glycine max), GmPGIP3, which is the most highly expressed gene of this family in the species, is phylogenetically grouped with PvPGIP1 and PvPGIP2, suggesting that the duplication that originated the ancestors of PvPGIP1/PvPGIP2 and PvPGIP3/PvPGIP4 occurred before the separation of Glycine and Phaseolus (Kalunke et al, 2014). Among these genes, PvPGIP2 is the most efficient in inhibiting the largest number of fungal PGs (Manfredini et al, 2005;D'Ovidio et al, 2004bD'Ovidio et al, , 2006. In addition, the highly conserved nature of the nucleotide sequence of this gene in various lines and species of Phaseolus indicates high adaptive significance (Farina et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Expression and validation of PvPGIP genes for resistance to white mold (Sclerotinia sclerotiorum) in common beans (Phaseolus vulgaris L.)

et al. 2016

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ABSTRACT. The interaction between polygalacturonase-inhibiting proteins (PGIPs), produced by plants, and endopolygalacturonases (PGs), produced by fungi, limits the destructive potential of PGs and can trigger plant defense responses. This study aimed to i) investigate variation in the expression of different common bean (Phaseolus vulgaris L.) genotypes and its relationship with resistance to white mold (Sclerotinia sclerotiorum); ii) determine the expression levels of PvPGIP genes at different time points after inoculation with white mold; and iii) investigate differences in PvPGIP gene expression between two white mold isolates with different levels of aggressiveness. Four bean lines were analyzed, including two lines from a recurrent selection for white mold (50/5 and 84/6), one resistant line that was not adapted to Brazilian conditions (Cornell 605), and one susceptible line (Corujinha). Gene expression was investigated at 0, 1, 2, 3, and 5 days after inoculation. The isolate UFLA 03 caused no significant difference in the relative expression of any gene examined, and was inefficient in discriminating among the genotypes. For the isolate UFLA 116, all of the genes were differentially expressed, as they were associated with resistance to white mold, and the expressions increased until the third day after inoculation. The 50/5 line was not significantly different from the Corujinha line for all of the genes analyzed. However, this line had a resistance level that was similar to that of Cornell 605, according to the straw test. Therefore, the incorporation of PvPGIP genes can increase the resistance of lines derived from recurrent selection.

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Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Expression and validation of PvPGIP genes for resistance to white mold (Sclerotinia sclerotiorum) in common beans (Phaseolus vulgaris L.)

et al. 2016

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“…PGs are important virulence factors for various fungi and bacteria, and a partial contribution of PGIPs to plant defense has been shown genetically using overexpression and gene silencing [22,23]. For example, B. cinerea BcPG1 is effectively inhibited by bean PvPGIP2 and PvPGIP2, and overexpression of these PGIPs in tobacco and Arabidopsis increases resistance to Botrytis infections [24]. Apart from directly suppressing PG activity, PGIPs are also thought to contribute to pathogen perception by preventing the degradation of oligogalacturonan elicitors that are released during infection [25].…”

Section: Wheat Inhibitor Xip-i Targets Fungal Gh11 and Gh10 Xylanasesmentioning

confidence: 99%

Enzyme–inhibitor interactions at the plant–pathogen interface

Misas-Villamil

Hoorn

2008

Current Opinion in Plant Biology

115

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The plant apoplast during plant-pathogen interactions is an ancient battleground that holds an intriguing range of attacking enzymes and counteracting inhibitors. Examples are pathogen xylanases and polygalacturonases that are inhibited by plant proteins like TAXI, XIP, and PGIP; and plant glucanases and proteases, which are targeted by pathogen proteins such as GIP1, EPI1, EPIC2B, and AVR2. These seven well-characterized inhibitors have different modes of action and many probably evolved from inactive enzymes themselves. Detailed studies of the structures, sequence variation, and mutated proteins uncovered molecular struggles between these enzymes and their inhibitors, resulting in positive selection for variant residues at the contact surface, where single residues determine the outcome of the interaction. Introduction Extracellular plant-pathogen interactions probably existed long before the evolution of pathogen effector translocation systems and plant resistance (R) genes. The molecular basis of these interactions is mostly undiscovered but some have been investigated in detail and reveal intriguing mechanisms. Here we will highlight major recent findings of extracellular enzyme-inhibitor interactions at the plant-pathogen interface.Although extracellular plant-pathogen interactions are complex, they can be simplified by assuming that they evolved in several stages (Figure 1). First, micro-organisms became pathogens by attacking plants using cell-wall-degrading enzymes and other hydrolases ( Figure 1A). In response to this attack, plants secrete inhibitors that suppress these hydrolases ( Figure 1B). Initially, these inhibitors were probably constitutively produced, but upon evolution of pathogen recognition systems the production and secretion of these proteins became inducible, becoming part of the arsenal of pathogenesis-related (PR) proteins. Besides suppression of pathogen attack, counter attack mechanisms also evolved in plants through the induced secretion of hydrolytic enzymes ( Figure 1C). Examples are the well-studied PR proteins including endo-b-1,3-glucanases (PR-2), chitinases (PR-3), and proteases (PR-7) [1 ]. Pathogens, in turn, responded to this counter attack by producing inhibitors that suppress these enzymes ( Figure 1D). The fifth and latest step was a sophisticated refinement of the pathogen recognition system by the evolution of R genes that recognize the manipulation of plant targets by pathogens, inducing a severe defense response that includes cell death ( Figure 1E). Aspects of this simplified model are consistent with the 'zigzag' model for the plant immune system, which explains the suppression of basal defense responses by pathogen effector proteins, followed by the evolution of efficient effector recognition by R proteins [2].Antagonistic interactions between organisms at the molecular level result in enzymes that evade inhibition, and inhibitors that adapt to these new enzymes. These 'molecular struggles' result in positive selection for variation of residues at the interactio...

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Evolution of Polygalacturonases and Polygalacturonase‐Inhibiting Proteins: A View Beyond the Classical Perspective

Haeger

Pauchet

Kirsch

2022

Annual Plant Reviews Online

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As the first line of defence, the plant cell wall represents a battleground for both attackers' arsenals of harmful compounds and defensive actions of plants. Plants counteract tissue maceration caused by their enemies' plant cell wall degrading enzymes. Among those, pectin‐degrading polygalacturonases (PGs) of the glycoside hydrolase family 28 (GH28) are impaired by PG‐inhibiting proteins (PGIPs), extracellular members of the leucine‐rich repeat (LRR) family. PG‐PGIP interaction is well studied in the context of microbial phytopathogens. However, hypothetically, every organism that benefits from PG activity could be affected by PGIPs. Herein, we develop this view from the plant, the insect and the evolutionary perspective: (i) Plants produce their own PGs, which are involved in different developmental processes. We revisit plant PG–PGIP interaction and discuss foundational studies in light of up‐to‐date plant PG amino acid sequence data. (ii) We summarise recent advances in the field of PGs produced by insects and insect‐associated microbial symbionts and review how PGIPs influence insect PGs. (iii) As the functions of PGIPs and closely related LRR proteins are not limited to the inhibition of PGs, we combine information on functionally characterised LRR proteins with a comprehensive phylogenetic analysis and discuss the roles of plant‐specific extracellular LRR proteins in plant resistance and beyond.

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Polygalacturonase-inhibiting protein 2 of Phaseolus vulgaris inhibits BcPG1, a polygalacturonase of Botrytis cinerea important for pathogenicity, and protects transgenic plants from infection

Cited by 78 publications

References 31 publications

Expression and validation of PvPGIP genes for resistance to white mold (Sclerotinia sclerotiorum) in common beans (Phaseolus vulgaris L.)

Expression and validation of PvPGIP genes for resistance to white mold (Sclerotinia sclerotiorum) in common beans (Phaseolus vulgaris L.)

Enzyme–inhibitor interactions at the plant–pathogen interface

Evolution of Polygalacturonases and Polygalacturonase‐Inhibiting Proteins: A View Beyond the Classical Perspective

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