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首页> 美国卫生研究院文献>Molecular Plant Pathology >The maize ZmMIEL1 E3 ligase and ZmMYB83 transcription factor proteins interact and regulate the hypersensitive defence response
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The maize ZmMIEL1 E3 ligase and ZmMYB83 transcription factor proteins interact and regulate the hypersensitive defence response

机译：玉米ZMMIEL1 E3连接酶和ZMMYB83转录因子蛋白相互作用和调节过敏防御反应

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The plant hypersensitive response (HR), a rapid cell death at the point of pathogenesis, is mediated by nucleotide‐binding site, leucine‐rich repeat (NLR) resistance proteins (R‐proteins) that recognize the presence of specific pathogen‐derived proteins. Rp1‐D21 is an autoactive maize NLR R‐protein that triggers HR spontaneously. We previously mapped loci associated with variation in the strength of HR induced by Rp1‐D21. Here we identify the E3 ligase ZmMIEL1 as the causal gene at a chromosome 10 modifier locus. Transient ZmMIEL1 expression in Nicotiana benthamiana reduced HR induced by Rp1‐D21, while suppression of ZmMIEL1 expression in maize carrying Rp1‐D21 increased HR. ZmMIEL1 also suppressed HR induced by another autoactive NLR, the Arabidopsis R‐protein RPM1D505V, in N. benthamiana. We demonstrated that ZmMIEL1 is a functional E3 ligase and that the effect of ZmMIEL1 was dependent on the proteasome but also that levels of Rp1‐D21 and RPM1D505V were not reduced when coexpressed with ZmMIEL1 in the N. benthamiana system. By comparison to a similar system in Arabidopsis, we identify ZmMYB83 as a potential target of ZmMIEL1. Suppression of ZmMYB83 expression in maize lines carrying Rp1‐D21 suppressed HR. Suppression of ZmMIEL1 expression caused an increase in ZmMYB83 transcript and protein levels in N. benthamiana and maize. Using coimmunoprecipitation and bimolecular fluorescence complementation assays, we demonstrated that ZmMIEL1 and ZmMYB83 physically interacted. Additionally, ZmMYB83 and ZmMIEL1 regulated the expression of a set of maize very long chain fatty acid (VLCFA) biosynthetic genes that may be involved in regulating HR.
机译：植物过敏反应（HR），在发病的点快速细胞死亡，通过识别特定病原体衍生的蛋白质的存在的核苷酸结合位点，富含亮氨酸重复（NLR）抗性蛋白（R-蛋白）介导的。 RP1-D21是一个autoactive玉米NLR R-蛋白触发HR自发。我们先前被映射的位点与由器Rp1-D21引起HR的强度变化相关联。在这里，我们在10号染色体修饰位点鉴定E3连接酶ZmMIEL1的因果基因。瞬时表达ZmMIEL1在由器Rp1-D21诱导本塞姆氏烟草减少HR，而在玉米承载器Rp1-D21 ZmMIEL1表达的抑制增加HR。 ZmMIEL1还抑制由另一个autoactive NLR，拟南芥R-蛋白RPM1D505V，在烟草本塞姆氏诱导HR。我们证明了ZmMIEL1是一个功能E3连接酶和ZmMIEL1的效果依赖于蛋白酶体，但也是器Rp1-D21和RPM1D505V水平时ZmMIEL1在烟草本塞姆氏中共表达系统并没有减少。通过比较在拟南芥中一个类似的系统，我们确定ZmMYB83作为ZmMIEL1的潜在目标。在承载器Rp1-D21的玉米品系ZmMYB83表达的抑制抑制HR。 ZmMIEL1表达的抑制导致在本塞姆氏烟草和玉米ZmMYB83转录物和蛋白水平的增加。采用免疫共沉淀和双分子荧光互补实验，我们证明了ZmMIEL1和ZmMYB83物理相互作用。此外，ZmMYB83和ZmMIEL1调节一组玉米非常长链脂肪酸（VLCFA）合成基因可以参与调节HR的表达。

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