Abstract

The resistance to Heterodera glycines 1 (Rhg1) locus is widely used by soybean breeders to reduce yield loss caused by soybean cyst nematode (SCN). α-SNAP (α-soluble NSF attachment protein) within Rhg1 locus contributes to SCN resistance by modulation of cell status at the SCN feeding site; however, the underlying mechanism is largely unclear. Here, we identified an α-SNAP-interacting protein, GmSYP31A, a Qa-SNARE (soluble NSF attachment protein receptor) protein from soybean. Expression of GmSYP31A significantly induced cell death in Nicotiana benthamiana leaves, and co-expression of α-SNAP and GmSYP31A could accelerate cell death. Overexpression of GmSYP31A increased SCN resistance, while silencing or overexpression of a dominant-negative form of GmSYP31A increased SCN sensitivity. GmSYP31A expression also disrupted endoplasmic reticulum-Golgi trafficking, and the exocytosis pathway. Moreover, α-SNAP was also found to interact with GmVDAC1D (voltage-dependent anion channel). The cytotoxicity induced by the expression of GmSYP31A could be relieved either with the addition of an inhibitor of VDAC protein, or by silencing the VDAC gene. Taken together, our data not only demonstrate that α-SNAP works together with GmSYP31A to increase SCN resistance through triggering cell death, but also highlight the unexplored link between the mitochondrial apoptosis pathway and vesicle trafficking.