The miR9863 family regulates distinct Mla alleles in barley to attenuate NLR receptor-triggered disease resistance and cell-death signaling.

The miR9863 family regulates distinct Mla alleles in barley to attenuate NLR receptor-triggered disease resistance and cell-death signaling.
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miR9863 家族调节大麦中不同的 Mla 等位基因以减弱 NLR 受体触发的疾病抗性和细胞死亡信号

DOI:
10.1371/journal.pgen.1004755
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发表时间:
2014-12
期刊:
影响因子:
4.5
通讯作者:
Shen QH
Shen QH
中科院分区:
生物学2区
文献类型:
--
作者:
Liu J;Cheng X;Liu D;Xu W;Wise R;Shen QH

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大麦(Hordeum vulgare L.)Mla等位基因编码卷曲螺旋(CC)、核苷酸结合、富含亮氨酸重复序列(NB-LRR)受体,该受体触发针对白粉病真菌(Blumeria graminis f.)大麦锈病菌(Bgh)。禾本科植物中Mla和NB-LRR基因在转录后水平的调控机制尚不清楚。microRNA家族miR 9863包括四个成员,其差异调节大麦中不同的Mla等位基因。我们表明,miR 9863成员指导大麦中Mla 1转录本的切割,并阻断或减少MLA 1蛋白在异源本氏烟草表达系统中的积累。调节特异性由成熟miR 9863家族成员中独特的单核苷酸多态性(SNP)的变化和Mla miR 9863结合位点中的两个SNP确定,所述Mla miR 9863结合位点将这些等位基因分成三组。此外,我们证明了22-nt miR 9863触发21-nt阶段siRNA(phasiRNA)的生物发生,并且这些sRNA一起形成用于抑制I组Mla等位基因表达的前馈调节网络。miR 9863成员的过表达特异性地减弱MLA 1,但不减弱MLA 10触发的疾病抗性和细胞死亡信号传导。我们提出了miR 9863家族在抑制大麦中一组MLA免疫受体引发的免疫应答信号传导中的关键作用。
Barley (Hordeum vulgare L.) Mla alleles encode coiled-coil (CC), nucleotide binding, leucine-rich repeat (NB-LRR) receptors that trigger isolate-specific immune responses against the powdery mildew fungus, Blumeria graminis f. sp. hordei (Bgh). How Mla or NB-LRR genes in grass species are regulated at post-transcriptional level is not clear. The microRNA family, miR9863, comprises four members that differentially regulate distinct Mla alleles in barley. We show that miR9863 members guide the cleavage of Mla1 transcripts in barley, and block or reduce the accumulation of MLA1 protein in the heterologous Nicotiana benthamiana expression system. Regulation specificity is determined by variation in a unique single-nucleotide-polymorphism (SNP) in mature miR9863 family members and two SNPs in the Mla miR9863-binding site that separates these alleles into three groups. Further, we demonstrate that 22-nt miR9863s trigger the biogenesis of 21-nt phased siRNAs (phasiRNAs) and together these sRNAs form a feed-forward regulation network for repressing the expression of group I Mla alleles. Overexpression of miR9863 members specifically attenuates MLA1, but not MLA10-triggered disease resistance and cell-death signaling. We propose a key role of the miR9863 family in dampening immune response signaling triggered by a group of MLA immune receptors in barley.
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