Glycine max polygalacturonase inhibiting protein 11 (GmPGIP11) functions in the root to suppress Heterodera glycines parasitism

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 which H. glycines
derives 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 specific G. max genotypes. Transcriptomic
analyses of RNA isolated from the syncytium undergoing
the process of defense have identified that one
of the 11 G. max PGIPs, GmPGIP11, is expressed during
defense. Functional transgenic analyses show roots undergoing
GmPGIP11 overexpression (OE) experience
an increase in its relative transcript abundance (RTA) as
compared to the ribosomal protein 21 (GmRPS21) control,
leading to a decrease in H. glycines parasitism as
compared to the overexpression control. The GmPGIP11
undergoing RNAi experiences a decrease in its RTA as
compared to the GmRPS21 control with transgenic roots
experiencing an increase in H. glycines parasitism as
compared to the RNAi control. Pathogen associated
molecular pattern (PAMP) triggered immunity (PTI)
and effector triggered immunity (ETI) components are
shown to influence GmPGIP11 expression while numerous
agricultural crops are shown to have homologs.