Poster: Plant-pathogen interactions

Abs # 575: Demonstration of activation for some EPG/PGIP combinations

Presenter:	Kemp, Gabre , gabre@ccrc.uga.edu
Authors	Kemp, Gabre  (A)   Bergmann, Carl W (A)
Affiliations:	(A): Complex Carbohydrate Research Center

The pectic polysaccharide rich middle lamella glues two adjacent plant cells together and is among the first cell wall components targeted by plant pathogenic fungi when gaining entry into the plant cell. This is achieved through endopolygalacturonases (EPGs) which hydrolyze non-esterified regions of wall-bound homogalacturonan that serves to expose non-pectic cell wall polymers to the action of other exo- and endoglycanases including the cellulases and hemicellulases. During pathogenesis, there is the potential for interaction between fungal EPGs and plant cell wall-located inhibitors of EPGs known as polygalacturonase inhibiting proteins (PGIPs) which are soluble glycoproteins, found in the extracellular matrix of dicotyledonous and monocotyledonous plants. Evidence to date indicates that PGIPs form high-affinity complexes with EPGs in a reversible, stoichiometrically defined manner.

Aspergillus niger encodes a family of seven different EPGs, two of these isoforms, termed PGA and PGB, are constitutively expressed. As part of an ongoing study of EPGs and PGIPs, we have recently obtained evidence that PGIPs may act as activators of some EPGs produced by A. niger. Micro-environmental parameters of the apoplast, such as variation in pH, appear to have the potential to alter the outcome of some EPG/PGIP interactions from inhibition to activation. These observations suggest a more complex regulatory mechanism in plant pathogenesis than was previously contemplated for EPG/PGIP interactions. In support of these observations we present the interaction of native P. vulgaris PGIP-2, recombinant P. Vulgaris PGIP-1, tomato PGIP and pear PGIP with five EPGs from A. niger.