Pant Shankar R, Krishnavajhala Aparna, McNeece Brant T, Lawrence Gary W, Klink Vincent P
a Department of Biological Sciences ; Mississippi State University ; Starkville , MS USA.
Plant Signal Behav. 2015;10(1):e977737. doi: 10.4161/15592324.2014.977737.
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.
实验表明，膜融合基因α可溶性 NSF 附着蛋白（α-SNAP）和 syntaxin 31（Gm-SYP38）有助于大豆抵御植物寄生线虫大豆胞囊线虫（Heterodera glycines）的感染。伴随着它们的表达，在水杨酸（SA）信号传导中起作用的防御基因增强疾病易感性 1（EDS1）和 PR1 非表达子（NPR1）会发生转录激活。这些结果表明抗凋亡环境响应基因损伤模拟疾病 1（LSD1）也参与了防御过程。在易感基因型大豆[Williams 82/PI 518671]中，经基因工程改造过表达大豆防御基因 Gm-α-SNAP、SYP38、EDS1、NPR1、葡萄孢诱导激酶 1（BIK1）和木葡聚糖内转糖基酶/水解酶（XTH）的根系，诱导了 Gm-LSD1（Gm-LSD1-2）的转录活性。在反向实验中，在易感基因型大豆[Williams 82/PI 518671]中经基因工程改造过表达 Gm-LSD1-2 的根系，在感染前诱导了 SYP38、EDS1、NPR1、BIK1 和 XTH 的表达水平，但未诱导α-SNAP 的表达。在研究 Gm-LSD1-2 在防御中的作用的试验中，其过表达导致线虫寄生率降低约 52%至 68%。相比之下，在抗性基因型大豆[北京/PI 548402]中对 Gm-LSD1-2 进行 RNA 干扰（RNAi），会使大豆胞囊线虫的寄生能力提高 3.24 至 10.42 倍。结果表明 Gm-LSD1-2 在大豆对大豆胞囊线虫寄生的防御反应中发挥作用。有人提出，LSD1 作为一种抗凋亡蛋白，可能营造了一种环境，使受保护的活植物细胞能够在寄生线虫附近分泌物质以解除其武装。在对线虫进行靶向失活后，随着受感染的根区域得到强化，被寄生的细胞会走向其靶向死亡。
