The resistance of sour orange to Citrus tristeza virus is mediated by both the salicylic acid and RNA silencing defence pathways

Citrus tristeza virus (CTV) induces in the field the decline and death of citrus varieties grafted on sour orange (SO) rootstock, which has forced the use of alternative decline‐tolerant rootstocks in affected countries, despite the highly desirable agronomic features of the SO rootstock. Declining citrus plants display phloem necrosis below the bud union. In addition, SO is minimally susceptible to CTV compared with other citrus varieties, suggesting partial resistance of SO to CTV. Here, by silencing different citrus genes with a Citrus leaf blotch virus‐based vector, we have examined the implication of the RNA silencing and salicylic acid (SA) defence pathways in the resistance of SO to CTV. Silencing of the genes RDR1, NPR1 and DCL2/DCL4, associated with these defence pathways, enhanced virus spread and accumulation in SO plants in comparison with non‐silenced controls, whereas silencing of the genes NPR3/NPR4, associated with the hypersensitive response, produced a slight decrease in CTV accumulation and reduced stunting of SO grafted on CTV‐infected rough lemon plants. We also found that the CTV RNA silencing suppressors p20 and p23 also suppress the SA signalling defence, with the suppressor activity being higher in the most virulent isolates.     

The gene encoding glutathione-dependent formaldehyde dehydrogenase/GSNO reductase is responsive to wounding,jasmonic acid and salicylic acid

It has recently been discovered that glutathione-dependent formaldehyde dehydrogenase (FALDH) exhibits a strong S-nitrosoglutathione reductase activity. Plants use NO and S-nitrosothiols as signaling molecules to activate defense mechanisms. Therefore, it is interesting to investigate the regulation of FALDH by mechanical wounding and plant hormones involved in signal transduction. Our results show that the gene encoding FALDH in Arabidopsis (ADH2) is down-regulated by wounding and activated by salicylic acid (SA). In tobacco, FALDH levels and enzymatic activity decreased after jasmonate treatment, and increased in response to SA. This is the first time that regulation of FALDH in response to signals associated with plant defense has been demonstrated.     

水杨酸诱导下蝙蝠蛾拟青霉转录组分析及虫草酸代谢途径关键酶基因挖掘

【目的】虫草酸是虫草中重要的活性成分之一,但其低含量极大地限制了其工业应用。水杨酸(salicylic acid, SA)是一种非生物诱导子,可以显著提高蝙蝠蛾拟青霉中虫草酸的合成,但蝙蝠蛾拟青霉虫草酸代谢途径及其对水杨酸的响应尚不明确。本研究旨在获得蝙蝠蛾拟青霉响应SA处理的转录组学信息,挖掘蝙蝠蛾拟青霉中虫草酸代谢途径关键酶基因。【方法】采用SA诱导培养蝙蝠蛾拟青霉,8 h后选取诱导和未诱导的菌丝进行转录组高通量测序分析。【结果】测序最终获得40.37 Gb的clean data,拼接得到20 317条unigene,平均长度为1 357.13 bp,功能注释共获得13 592条unigene。差异基因分析共筛选出差异基因2 574个,其中有1 135个上调,1 439个下调。KEGG富集分析表明,差异基因主要富集于细胞周期、减数分裂、半乳糖代谢、DNA复制、糖醇脂类生物合成、甘油脂类代谢等KEGG通路中。进一步分析得到与虫草酸代谢相关的基因13条,其中参与虫草酸生物合成的基因glk、gpi、gla、mpi、fbp、mtld在SA处理后表达量上调,而涉及虫草酸消耗的基因mdh在SA...     

The Arabidopsis ssi1 mutation restores pathogenesis-related gene expression in npr1 plants and renders defensin gene expression salicylic acid dependent.

The Arabidopsis NPR1 gene was previously shown to be required for the salicylic acid (SA)- and benzothiadiazole (BTH)-induced expression of pathogenesis-related (PR) genes and systemic acquired resistance. The dominant ssi1 (for suppressor of SA insensitivity) mutation characterized in this study defines a new component of the SA signal transduction pathway that bypasses the requirement of NPR1 for expression of the PR genes and disease resistance. The ssi1 mutation caused PR (PR-1, BGL2 [PR-2], and PR-5) genes to be constitutively expressed and restored resistance to an avirulent strain of Pseudomonas syringae pv tomato in npr1-5 (previously called sai1) mutant plants. In addition, ssi1 plants were small, spontaneously developed hypersensitive response-like lesions, accumulated elevated levels of SA, and constitutively expressed the antimicrobial defensin gene PDF1.2. The phenotypes of the ssi1 mutant are SA dependent. When SA accumulation was prevented in ssi1 npr1-5 plants by expressing the SA-degrading salicylate hydroxylase (nahG) gene, all of the phenotypes associated with the ssi1 mutation were suppressed. However, lesion formation and expression of the PR genes were restored in these plants by the application of BTH. Interestingly, expression of PDF1.2, which previously has been shown to be SA independent but jasmonic acid and ethylene dependent, was also suppressed in ssi1 npr1-5 plants by the nahG gene. Furthermore, exogenous application of BTH restored PDF1.2 expression in these plants. Our results suggest that SSI1 may function as a switch modulating cross-talk between the SA- and jasmonic acid/ethylene-mediated defense signal transduction pathways.     

The Arabidopsis extensin gene is developmentally regulated, is induced by wounding, methyl jasmonate, abscisic and salicylic acid, and codes for a protein with unusual motifs

A single-copy extensin gene (atExt1) has been isolated from Arabidopsis thaliana (L.) Heynh. The deduced amino acid sequence consists of 374 amino acids which are organised into highly ordered repeating blocks in which Ser(Pro)₄ and Ser(Pro)₃ motifs alternate. Two copies of the Tyr-X-Tyr-Lys motif and 13 copies of the Val-Tyr-Lys motif are present, showing that this extensin may be highly cross-linked, possessing the capacity for both intra and inter-molecular bond formation. The gene atExt1 is normally expressed in the root and is silent in the leaf; wounding reverses this pattern, turning on the gene in the leaf and repressing it in the root. The promoter contains motifs which have been found to activate plant defence genes in response to salicylic acid, abscisic acid and methyl jasmonate; when these compounds are applied to the roots, the atExt1 gene is activated in the leaf. Received: 11 September 1998 / Accepted: 20 December 1998     

Harpin induces disease resistance in Arabidopsis through the systemic acquired resistance pathway mediated by salicylic acid and the NIM1 gene

Harpin, the product of the hrpN gene of Erwinia amylovora, elicits the hypersensitive response and disease resistance in many plants. Harpin and known inducers of systemic acquired resistance (SAR) were tested on five genotypes of Arabidopsis thaliana to assess the role of SAR in harpin-induced resistance. In wild-type plants, harpin elicited systemic resistance to Peronospora parasitica and Pseudomonas syringae pv. tomato, accompanied by induction of the SAR genes PR-1 and PR-2. However, in experiments with transgenic Arabidopsis plants containing the nahG gene which prevents accumulation of salicylic acid (SA), harpin neither elicited resistance nor activated SAR gene expression. Harpin also failed to activate SAR when applied to nim1 (non-inducible immunity) mutants, which are defective in responding to SA and regulation of SAR. In contrast, mutants compromised in responsiveness to methyl jasmonate and ethylene developed the same resistance as did wild-type plants. Thus, harpin elicits disease resistance through the NIM1-mediated SAR signal transduction pathway in an SA-dependent fashion. The site of action of harpin in the SAR regulatory pathway is upstream of SA.