Experiments show the membrane fusion genes α soluble NSF attachment protein (α-SNAP) and syntaxin 31 (Gm-SYP38) contribute to the ability of Glycine max to defend itself from infection by the plant parasitic nematode Heterodera glycines. Accompanying their expression is the transcriptional activation of the defense genes ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and NONEXPRESSOR OF PR1 (NPR1) that function in salicylic acid (SA) signaling. These results implicate the added involvement of the antiapoptotic, environmental response gene LESION SIMULATING DISEASE1 (LSD1) in defense. Roots engineered to overexpress the G. max defense genes Gm-α-SNAP, SYP38, EDS1, NPR1, BOTRYTIS INDUCED KINASE1 (BIK1) and xyloglucan endotransglycosylase/hydrolase (XTH) in the susceptible genotype G. max[Williams 82/PI 518671] have induced Gm-LSD1 (Gm-LSD1-2) transcriptional activity. In reciprocal experiments, roots engineered to overexpress Gm-LSD1-2 in the susceptible genotype G. max[Williams 82/PI 518671] have induced levels of SYP38, EDS1, NPR1, BIK1 and XTH, but not α-SNAP prior to infection. In tests examining the role of Gm-LSD1-2 in defense, its overexpression results in ∼52 to 68% reduction in nematode parasitism. In contrast, RNA interference (RNAi) of Gm-LSD1-2 in the resistant genotype G. max[Peking/PI 548402] results in an 3.24-10.42 fold increased ability of H. glycines to parasitize. The results identify that Gm-LSD1-2 functions in the defense response of G. max to H. glycines parasitism. It is proposed that LSD1, as an antiapoptotic protein, may establish an environment whereby the protected, living plant cell could secrete materials in the vicinity of the parasitizing nematode to disarm it. After the targeted incapacitation of the nematode the parasitized cell succumbs to its targeted demise as the infected root region is becoming fortified.
Keywords: BIK1, botrytis induced kinase1; CuSOD, copper superoxide dismutase; EDS1, enhanced disease susceptibility1; ER, endoplasmic reticulum; GOI, gene of interest; Golgi; INA, 2,6-dichloroisonicotinic acid; JA, jasmonic acid; LESION SIMULATING DISEASE1 (LSD1); LOL1, LSD1-like; LSD1, lesion simulating disease1; MATE, multidrug and toxin extrusion; NPR1, nonexpressor of PR1; O2−, superoxide; PAD4, phytoalexin deficient 4; PCD, programmed cell death; PR1, pathogenesis-related 1; RNAi, RNA interference; ROI, reactive oxygen intermediates; SA, salicylic acid; SAR, systemic acquired resistance; SHMT, serine hydroxymethyltransferase; SID2, salicylic-acid-induction deficient2; Sed5p, suppressors of the erd2-deletion 5; XTH, xyloglucan endotransglycosylase/hydrolase; membrane fusion; pathogen resistance; qPCR, quantitative polymerase chain reaction; salicylic acid; sec, secretion; signaling; syntaxin 31; vesicle; α-SNAP, alpha soluble N-ethylmaleimide-sensitive factor attachment protein.