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ERF5 和 ERF6 作为 JA/Et 介导的拟南芥对灰葡萄孢防御的正调控因子,发挥冗余作用。

ERF5 and ERF6 play redundant roles as positive regulators of JA/Et-mediated defense against Botrytis cinerea in Arabidopsis.

机构信息

School of Biological and Biomedical Sciences, Durham Centre for Crop Improvement Technology, Durham University, Durham, United Kingdom.

出版信息

PLoS One. 2012;7(4):e35995. doi: 10.1371/journal.pone.0035995. Epub 2012 Apr 26.

DOI:10.1371/journal.pone.0035995
PMID:22563431
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3338558/
Abstract

The ethylene response factor (ERF) family in Arabidopsis thaliana comprises 122 members in 12 groups, yet the biological functions of the majority remain unknown. Of the group IX ERFs, the IXc subgroup has been studied the most, and includes ERF1, ERF14 and ORA59, which play roles in plant innate immunity. Here we investigate the biological functions of two members of the less studied IXb subgroup: ERF5 and ERF6. In order to identify potential targets of these transcription factors, microarray analyses were performed on plants constitutively expressing either ERF5 or ERF6. Expression of defense genes, JA/Et-responsive genes and genes containing the GCC box promoter motif were significantly upregulated in both ERF5 and ERF6 transgenic plants, suggesting that ERF5 and ERF6 may act as positive regulators of JA-mediated defense and potentially overlap in their function. Since defense against necrotrophic pathogens is generally mediated through JA/Et-signalling, resistance against the fungal necrotroph Botrytis cinerea was examined. Constitutive expression of ERF5 or ERF6 resulted in significantly increased resistance. Although no significant difference in susceptibility to B. cinerea was observed in either erf5 or erf6 mutants, the erf5 erf6 double mutant showed a significant increase in susceptibility, which was likely due to compromised JA-mediated gene expression, since JA-induced gene expression was reduced in the double mutant. Taken together these data suggest that ERF5 and ERF6 play positive but redundant roles in defense against B. cinerea. Since mutual antagonism between JA/Et and salicylic acid (SA) signalling is well known, the UV-C inducibility of an SA-inducible gene, PR-1, was examined. Reduced inducibilty in both ERF5 and ERF6 constitutive overexepressors was consistent with suppression of SA-mediated signalling, as was an increased susceptibility to avirulent Pseudomonas syringae. These data suggest that ERF5 and ERF6 may also play a role in the antagonistic crosstalk between the JA/Et and SA signalling pathways.

摘要

拟南芥中的乙烯响应因子(ERF)家族包含 12 个亚家族的 122 个成员,但大多数的生物学功能仍未知。在第 IX 组 ERFs 中,IXc 亚组的研究最多,包括 ERF1、ERF14 和 ORA59,它们在植物先天免疫中发挥作用。在这里,我们研究了研究较少的 IXb 亚组的两个成员 ERF5 和 ERF6 的生物学功能。为了鉴定这些转录因子的潜在靶标,对组成型表达 ERF5 或 ERF6 的植物进行了微阵列分析。在 ERF5 和 ERF6 转基因植物中,防御基因、JA/Et 响应基因和含有 GCC 框启动子模体的基因的表达均显著上调,表明 ERF5 和 ERF6 可能作为 JA 介导的防御的正调节剂,并且它们的功能可能重叠。由于对坏死型病原体的防御通常是通过 JA/Et 信号传导介导的,因此检查了真菌坏死型病原体 Botrytis cinerea 的抗性。组成型表达 ERF5 或 ERF6 导致抗性显著增强。尽管在 erf5 或 erf6 突变体中观察到对 B. cinerea 的敏感性没有显着差异,但 erf5 erf6 双突变体的敏感性显着增加,这可能是由于 JA 介导的基因表达受损所致,因为在双突变体中 JA 诱导的基因表达减少。总之,这些数据表明 ERF5 和 ERF6 在抵抗 B. cinerea 中发挥积极但冗余的作用。由于 JA/Et 和水杨酸(SA)信号之间的相互拮抗作用是众所周知的,因此检查了 SA 诱导基因 PR-1 的 UV-C 诱导性。在 ERF5 和 ERF6 组成型过表达物中,诱导性降低与 SA 介导的信号转导的抑制一致,对无毒假单胞菌的敏感性增加也是如此。这些数据表明 ERF5 和 ERF6 也可能在 JA/Et 和 SA 信号通路之间的拮抗串扰中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/721c6e51b992/pone.0035995.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/b1ba6657f205/pone.0035995.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/9f33e64e8de6/pone.0035995.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/6dc36fc17800/pone.0035995.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/96ed6ab7d4e7/pone.0035995.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/4e8838bc9369/pone.0035995.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/64bf169e7277/pone.0035995.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/721c6e51b992/pone.0035995.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/b1ba6657f205/pone.0035995.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/9f33e64e8de6/pone.0035995.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/6dc36fc17800/pone.0035995.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/96ed6ab7d4e7/pone.0035995.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/4e8838bc9369/pone.0035995.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/64bf169e7277/pone.0035995.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26db/3338558/721c6e51b992/pone.0035995.g007.jpg

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