Glycine maxpolygalacturonase inhibiting protein 11 (GmPGIP11) functions in the root to suppressHeterodera glycinesparasitism

Abstract

Pathogen-secreted polygalacturonases (PGs) alter plant cell wall structure by cleaving the α- (1→4) linkages between D-galacturonic acid residues in homogalacturonan (HG), macerating the cell wall, facilitating infection. Plant PG inhibiting proteins (PGIPs) disengage pathogen PGs, impairing infection. The soybean cyst nematode,Heterodera glycines,obligate root parasite produces secretions, generating a multinucleate nurse cell called a syncytium, a byproduct of the merged cytoplasm of 200-250 root cells, occurring through cell wall maceration. The common cytoplasmic pool, surrounded by an intact plasma membrane, provides a source from whichH. glycinesderives nourishment but without killing the parasitized cell during a susceptible reaction. The syncytium is also the site of a naturally-occurring defense response that happens in specificG. maxgenotypes. Transcriptomic analyses of RNA isolated from the syncytium undergoing the process of defense have identified that one of the 11G. max PGIPs,GmPGIP11, is expressed during defense. Functional transgenic analyses show roots undergoingGmPGIP11overexpression (OE) experience an increase in its relative transcript abundance (RTA) as compared to theribosomal protein 21(GmRPS21) control, leading to a decrease inH. glycinesparasitism as compared to the overexpression control. TheGmPGIP11undergoing RNAi experiences a decrease in its RTA as compared to theGmRPS21control with transgenic roots experiencing an increase inH. glycinesparasitism as compared to the RNAi control. Pathogen associated molecular pattern (PAMP) triggered immunity (PTI) and effector triggered immunity (ETI) components are shown to influenceGmPGIP11expression while numerous agricultural crops are shown to have homologs.