A Qa-SNARE complex protein contributes to soybean cyst nematode resistance through regulation of mitochondria-mediated cell death.

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 health at SCN feeding site, however, the corresponding mechanism is largely unclear. Here, we identified an α-SNAP-interacting protein, GmSYP31A, a Qa-SNARE protein from soybean. Expression of GmSYP31A significantly induced cell death in Nicotiana benthamiana leaves, and co-expression of α-SNAP and GmSYP31A could accelerate the cell death. Overexpression of GmSYP31A increased SCN resistance, while silencing of GmSYP31A or overexpression of a dominant-negative form of GmSYP31A increased SCN sensitivity. ER-Golgi trafficking and exocytosis pathway is disrupted by GmSYP31A expression. Moreover, α-SNAP was also detected to interact with GmVDAC1D (Voltage-Dependent Anion Channel). The cytotoxicity induced by the expression of GmSYP31A could be relieved either with the addition of DIDS, an inhibitor of VDAC protein, or by silencing VDAC gene via TRV-VIGS system. Taken together, our data not only provide valuable information that α-SNAP works together with GmSYP31A to increase SCN resistance through triggering cell death, but also highlight the unexplored link between the mitochondria apoptosis pathway and the vesicle trafficking.