An update on polygalacturonase-inhibiting protein (PGIP), a leucine-rich repeat protein that protects crop plants against pathogens

Abstract

Polygalacturonase inhibiting proteins (PGIPs) are cell wall proteins that inhibit the pectin-depolymerizing activity of polygalacturonases secreted by microbial pathogens and insects. These ubiquitous inhibitors have a leucine-rich repeat structure that is strongly conserved in monocot and dicot plants. Previous reviews have summarized the importance of PGIP in plant defense and the structural basis of PG-PGIP interaction; here we update the current knowledge about PGIPs with the recent findings on the composition and evolution of pgip gene families, with a special emphasis on legume and cereal crops. We also update the information about the inhibition properties of single pgip gene products against microbial PGs and the results, including field tests, showing the capacity of PGIP to protect crop plants against fungal, oomycetes and bacterial pathogens.

Keywords: bacterial pathogens; fungal pathogens; gene family; plant protection; polygalacturonase inhibiting proteins (PGIPs); transgenic plants.

Figure 1

Schematic representation of the genomic organization pgip families in rice, wheat, bean, soybean, chickpea, barrel clover and thale cress. Each block-arrow with compound-type lines represents a predicted pgip gene and a block-arrow with dash type lines represents a predicted pseudo-gene or remnant gene. Vertical line within block-arrow indicates introns (Capgip2, Atpgip1, and Atpgip2) or a Copia retrotransposon (Tapgip3). The direction of the arrow indicates ATG to stop codon. The location of pgip genes of legume species are based on Kalunke et al. (2014), those of rice and wheat on Janni et al. (2006) and Di Giovanni et al. (2008), and those of thale crest on Ferrari et al. (2003). Chr, chromosome.

Figure 2

A model for the role of PGIP in the defense response against pathogens. Delay of symptoms is related to the inhibitory activity of PGIP toward PGs secreted by the pathogens and likely to the accumulation of oligogalacturonide (OG) elicitors, which are recognized by WAK1 and likely other receptors not yet characterized. Cell wall modification and pectin shielding could also play a role. Signaling cascades activated by OGs are described in Ferrari et al. (2013).