Role of Rhg1-encoded α-SNAPs in Rhg1-Mediated Resistance to Soybean Cyst Nematode    
A. BAYLESS (1), J. Smith (1), J. Song (1), P. McMinn (1), A. Bent (1), UW-Madison, U.S.A.

Heterodera glycines (Soybean cyst nematode, SCN) is a highly adapted, obligate parasite of soybean that reprograms root cells to form a metabolically hyperactive nematode feeding site termed a syncytium. This causes major soybean yield losses every year. The Rhg1 locus is the primary means of reducing yield loss caused by SCN. The most widely used Rhg1 locus consists of ten tandem repeats of a ~30 kb block that encodes four genes. However, the molecular mechanisms of Rhg1-mediated resistance remain unclear. Our recent work revealed that resistance-conferring Rhg1 loci group into two classes, carrying either a high or intermediate Rhg1 copy number and also encoding distinct α-SNAP proteins. α-SNAPs bind to cis-SNARE complexes and stimulate their disassembly by the ATPase, NSF. The regeneration of free SNAREs by α-SNAP and NSF is necessary for future rounds of vesicle fusion. Both classes of Rhg1 encode α-SNAPs with unusual C-terminal amino acid polymorphisms at functionally important positions. We have utilized in vitro and in vivo approaches to determine how Rhg1-encoded α-SNAPs differ from wild type α-SNAPs as well as to uncover specific roles during Rhg1 mediated SCN resistance. Our data reveal that these variant, resistance-conferring Rhg1 α-SNAPs are defective yet sufficiently conserved to disrupt wild-type α-SNAP activity, suggesting competitive disruption of normal vesicle trafficking as an important mechanism of plant disease resistance.

Abstract Number: C17-3, P7-226
Session Type: Concurrent