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SUMO modification of LBD30 by SIZ1 regulates secondary cell wall formation in Arabidopsis thaliana

机译:SIZ1对LBD30的SUMO修饰调节拟南芥中次生细胞壁的形成

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摘要

A wide range of biological processes are regulated by sumoylation, a post-translational modification involving the conjugation of SUMO (Small Ubiquitin-Like Modifier) to protein. In Arabidopsis thaliana, AtSIZ1 encodes a SUMO E3 ligase for SUMO modification. siz1 mutants displayed defective secondary cell walls (SCWs) in inflorescence fiber cells. Such defects were caused by repression of SND1/NST1-mediated transcriptional networks. Yeast two-hybrid assay indicated that SIZ1 interacts with the LBD30 C-terminal domain, which was further confirmed using bimolecular fluorescence complementation and immunoprecipitation. Mass spectrometry and co-immunoprecipitation indicated that SIZ1 mediates SUMO conjugation to LBD30 at the K226 residue. Genes controlling SCW formation were activated by the overexpression of LBD30, but not in the LBD30(K226R) mutant. LBD30 enhancement of SCW formation resulted from upregulation of SND1/NST1-mediated transcriptional networks. This study presents a mechanism by which sumoylation of LBD30, mediated by SIZ1, regulates SCW formation in A. thaliana.
机译:sumoylation调节了广泛的生物学过程,sumoylation是一种翻译后修饰,涉及SUMO(小泛素样修饰剂)与蛋白质的缀合。在拟南芥中,AtSIZ1编码用于SUMO修饰的SUMO E3连接酶。 siz1突变体显示花序纤维细胞中的次生细胞壁(SCWs)有缺陷。此类缺陷是由SND1 / NST1介导的转录网络的阻遏引起的。酵母双杂交试验表明SIZ1与LBD30 C末端结构域相互作用,这已通过双分子荧光互补和免疫沉淀进一步证实。质谱和免疫共沉淀表明SIZ1介导SUMO与K226残基的LBD30结合。控制SCW形成的基因被LBD30的过表达激活,但不在LBD30(K226R)突变体中激活。 LBD30增强SCW形成的原因是SND1 / NST1介导的转录网络上调。这项研究提出了一种机制,SIZ1介导的LBD30的磺酰化调节了拟南芥中SCW的形成。

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