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茉莉酸和乙烯依赖的防御基因表达和真菌毒性因子的抑制:小麦赤霉病抗性的两个重要机制?

Jasmonate and ethylene dependent defence gene expression and suppression of fungal virulence factors: two essential mechanisms of Fusarium head blight resistance in wheat?

机构信息

Department of Plant Breeding, Justus-Liebig University, Institute of Agronomy and Plant Breeding I, Giessen, Germany.

出版信息

BMC Genomics. 2012 Aug 2;13:369. doi: 10.1186/1471-2164-13-369.

DOI:10.1186/1471-2164-13-369
PMID:22857656
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3533685/
Abstract

BACKGROUND

Fusarium head blight (FHB) caused by Fusarium species like F. graminearum is a devastating disease of wheat (Triticum aestivum) worldwide. Mycotoxins such as deoxynivalenol produced by the fungus affect plant and animal health, and cause significant reductions of grain yield and quality. Resistant varieties are the only effective way to control this disease, but the molecular events leading to FHB resistance are still poorly understood. Transcriptional profiling was conducted for the winter wheat cultivars Dream (moderately resistant) and Lynx (susceptible). The gene expressions at 32 and 72 h after inoculation with Fusarium were used to trace possible defence mechanisms and associated genes. A comparative qPCR was carried out for selected genes to analyse the respective expression patterns in the resistant cultivars Dream and Sumai 3 (Chinese spring wheat).

RESULTS

Among 2,169 differentially expressed genes, two putative main defence mechanisms were found in the FHB-resistant Dream cultivar. Both are defined base on their specific mode of resistance. A non-specific mechanism was based on several defence genes probably induced by jasmonate and ethylene signalling, including lipid-transfer protein, thionin, defensin and GDSL-like lipase genes. Additionally, defence-related genes encoding jasmonate-regulated proteins were up-regulated in response to FHB. Another mechanism based on the targeted suppression of essential Fusarium virulence factors comprising proteases and mycotoxins was found to be an essential, induced defence of general relevance in wheat. Moreover, similar inductions upon fungal infection were frequently observed among FHB-responsive genes of both mechanisms in the cultivars Dream and Sumai 3.

CONCLUSIONS

Especially ABC transporter, UDP-glucosyltransferase, protease and protease inhibitor genes associated with the defence mechanism against fungal virulence factors are apparently active in different resistant genetic backgrounds, according to reports on other wheat cultivars and barley. This was further supported in our qPCR experiments on seven genes originating from this mechanism which revealed similar activities in the resistant cultivars Dream and Sumai 3. Finally, the combination of early-stage and steady-state induction was associated with resistance, while transcript induction generally occurred later and temporarily in the susceptible cultivars. The respective mechanisms are attractive for advanced studies aiming at new resistance and toxin management strategies.

摘要

背景

由镰刀菌属真菌(如禾谷镰刀菌)引起的小麦赤霉病(FHB)是一种世界性的小麦毁灭性疾病。真菌产生的真菌毒素如脱氧雪腐镰刀菌烯醇会影响植物和动物健康,并导致谷物产量和质量的显著下降。抗性品种是控制这种疾病的唯一有效方法,但导致 FHB 抗性的分子事件仍知之甚少。对冬小麦品种 Dream(中度抗性)和 Lynx(易感性)进行了转录谱分析。在接种镰刀菌后 32 和 72 小时,使用基因表达来追踪可能的防御机制和相关基因。对选定基因进行了比较 qPCR 分析,以分析抗性品种 Dream 和 Sumai 3(中国春小麦)中的各自表达模式。

结果

在 2169 个差异表达基因中,在 FHB 抗性品种 Dream 中发现了两种可能的主要防御机制。这两种机制都是基于它们特定的抗性模式定义的。一种非特异性机制是基于几种防御基因,这些基因可能是由茉莉酸和乙烯信号诱导的,包括脂质转移蛋白、硫肽、防御素和 GDSL 样脂肪酶基因。此外,与 FHB 反应相关的基因编码茉莉酸调控蛋白,这些基因被上调以响应 FHB。另一种机制是基于靶向抑制真菌毒力因子,包括蛋白酶和真菌毒素,这是小麦中一种重要的、普遍相关的诱导防御机制。此外,在 Dream 和 Sumai 3 两种机制的 FHB 响应基因中,经常观察到类似的真菌感染诱导。

结论

根据其他小麦品种和大麦的报道,与防御真菌毒力因子的机制相关的 ABC 转运蛋白、UDP-葡萄糖基转移酶、蛋白酶和蛋白酶抑制剂基因在不同的抗性遗传背景下显然是活跃的。在我们对该机制的七个基因的 qPCR 实验中,也得到了进一步的支持,这些基因在抗性品种 Dream 和 Sumai 3 中表现出相似的活性。最后,早期和稳定期诱导的结合与抗性有关,而在易感品种中,转录诱导通常发生得更晚且暂时。这些机制对于旨在开发新的抗性和毒素管理策略的深入研究具有吸引力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a3/3533685/6cb65c9d5c2f/1471-2164-13-369-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a3/3533685/ec637734ff13/1471-2164-13-369-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a3/3533685/1299f14021d2/1471-2164-13-369-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a3/3533685/4b852c5ec177/1471-2164-13-369-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a3/3533685/6cb65c9d5c2f/1471-2164-13-369-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a3/3533685/ec637734ff13/1471-2164-13-369-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a3/3533685/1299f14021d2/1471-2164-13-369-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a3/3533685/4b852c5ec177/1471-2164-13-369-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79a3/3533685/6cb65c9d5c2f/1471-2164-13-369-4.jpg

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