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串联重复拷贝数调控大麦白粉病抗性的生理变化。

Physiological Changes in Barley Powdery Mildew Resistance Conditioned by Tandem Repeat Copy Number.

机构信息

Centre for Crop and Disease Management, School of Molecular and Life Sciences, Curtin University, Bentley, WA 6102, Australia.

Centre Queensland Alliance for Agriculture and Food Innovation, The University of Queensland, St. Lucia, QLD 4069, Australia.

出版信息

Int J Mol Sci. 2020 Nov 20;21(22):8769. doi: 10.3390/ijms21228769.

DOI:10.3390/ijms21228769
PMID:33233522
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7699567/
Abstract

Wild barley accessions have evolved broad-spectrum defence against barley powdery mildew through recessive mutations. However, the defence response is associated with deleterious phenotypes with a cost to yield and fertility, with implications for natural fitness and agricultural productivity. This research elucidates the mechanism behind a novel allele, designated (), which has a milder phenotype compared to standard . Bisulphite sequencing and histone ChIP-seq analyses using near-isogenic lines showed pronounced repression of the promoter in standard compared to (), with repression governed by 24 nt heterochromatic small interfering RNAs. The () allele appears to largely reduce the physiological effects of while still endorsing a high level of powdery mildew resistance. RNA sequencing showed that this is achieved through only partly restricted expression of , allowing adequate temporal induction of defence genes during infection and expression close to wild-type levels in the absence of infection. The two alleles showed copy number proportionate oxidase and peroxidase expression levels during infection, but lower amino acid and aromatic compound biosynthesis compared to the null allele . Examination of highly expressed genes revealed a common WRKY W-box binding motif (consensus ACCCGGGACTAAAGG) and a transcription factor more highly expressed in resistance. In conclusion, () appears to significantly mitigate the trade-off between defence and normal gene expression.

摘要

野生大麦通过隐性突变进化出广谱防御能力来抵御大麦白粉病。然而,这种防御反应与有害表型相关,会降低产量和繁殖力,对自然适应性和农业生产力有影响。本研究阐明了一个新等位基因()背后的机制,与标准等位基因()相比,该等位基因表现出更温和的表型。利用近等基因系进行亚硫酸氢盐测序和组蛋白 ChIP-seq 分析表明,与()相比,标准()中 启动子受到强烈抑制,这种抑制受 24 个核苷酸异染色质小干扰 RNA 调控。与标准等位基因相比,()等位基因似乎在很大程度上降低了 对生理的影响,但仍能保持高水平的白粉病抗性。RNA 测序表明,这是通过不完全限制 的表达来实现的,从而在感染期间充分诱导防御基因的表达,并在没有感染的情况下使表达接近野生型 水平。两个 等位基因在感染期间表现出与氧化酶和过氧化物酶表达水平成比例的拷贝数,但与缺失等位基因相比,氨基酸和芳香族化合物生物合成水平较低。对高表达基因的研究表明,存在一个共同的 WRKY W-盒结合基序(保守的 ACCCGGGACTAAAGG)和一个在抗性中表达更高的转录因子。总之,()似乎显著减轻了防御和正常基因表达之间的权衡。

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