The bacterial effector harpin induces the transcription of the Arabidopsis thaliana NON-RACE SPECIFIC DISEASE RESISTANCE 1/HARPIN INDUCED1 (NDR1/HIN1) coiled-coil nucleotide binding leucine rich repeat (CC-NB-LRR) defense signaling gene. In Glycine max, Gm-NDR1-1 transcripts have been detected within root cells undergoing a natural resistant reaction to parasitism by the syncytium-forming nematode Heterodera glycines, functioning in the defense response. Expressing Gm-NDR1-1 in Gossypium hirsutum leads to resistance to Meloidogyne incognita parasitism. In experiments presented here, the heterologous expression of Gm-NDR1-1 in G. hirsutum impairs Rotylenchulus reniformis parasitism. These results are consistent with the hypothesis that Gm-NDR1-1 expression functions broadly in generating a defense response. To examine a possible relationship with harpin, G. max plants topically treated with harpin result in induction of the transcription of Gm-NDR1-1. The result indicates the topical treatment of plants with harpin, itself, may lead to impaired nematode parasitism. Topical harpin treatments are shown to impair G. max parasitism by H. glycines, M. incognita and R. reniformis and G. hirsutum parasitism by M. incognita and R. reniformis. How harpin could function in defense has been examined in experiments showing it also induces transcription of G. max homologs of the proven defense genes ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1), TGA2, galactinol synthase, reticuline oxidase, xyloglucan endotransglycosylase/hydrolase, alpha soluble N-ethylmaleimide-sensitive fusion protein (α-SNAP) and serine hydroxymethyltransferase (SHMT). In contrast, other defense genes are not directly transcriptionally activated by harpin. The results indicate harpin induces pathogen associated molecular pattern (PAMP) triggered immunity (PTI) and effector-triggered immunity (ETI) defense processes in the root, activating defense to parasitic nematodes.
Syntaxin proteins are involved in the process of membrane fusion. G. max syntaxin genes (Gm-SYP22-3, and GmSYP22-4) that were similar in amino acid composition have been found to contribute to the ability of Glycine max to defend itselffrom infection by the plant- parasitic nematode Rotylenchulus reniformis. The Gm-SYP22-3and Gm-SYP22-4 genes were expressed in root cells (syncytia) undergoing a resistant reaction while not being expressed in control cells. The Gm-SYP22-3 and Gm-SYP22-4 genes have been isolated from genetically engineered in G. max [Williams 82/PI518671], a genotype typically susceptible to R. reniformis parasitism. Genetically engineered plants in G. max [Williams 82/PI 518671] that lack the overexpression of Gm-SYP22-3 or Gm-SYP22-4 genes have also been produced to serve as a control. The transgenic Gm-SYP22-3 or Gm-SYP22-4 overexpression lines with their pRAP15 control have then been infected with R. reniformis. Infection was allowed to proceed for 30 days. At the end of the 30-day life span, R. reniformisstages were extracted from the soil and eggs from the roots, enumerated and compared to control plants. Plants overexpressing Gm-SYP22-3 or Gm-SYP22-4 had suppressed R. reniformis. In contrast, the gene expression levels of Gm-SYP22-3 and Gm-SYP22-4 were reduced in transgenic lines engineered for their RNA interference (RNAi) in G. max [Peking/PI 548402], a genotype normally resistant to R. reniformis. In comparison to genetically engineered control G. max [Peking/PI 548402] lines, RNAi of Gm-SYP22-3 or Gm-SYP22-4 resulted in an increase in parasitism in the normally R. reniformis resistant G. max [Peking/PI 548402].
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