Specific control of Arabidopsis BAK1/SERK4-regulated cell death by protein glycosylation.
Specific control of Arabidopsis BAK1/SERK4-regulated cell death by protein glycosylation.
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通过蛋白质糖基化对拟南芥BAK1/SERK4调节的细胞死亡的特定控制。
DOI：
10.1038/nplants.2015.218
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发表时间：
2016-01-25
期刊：
影响因子：
18
通讯作者：
He P
中科院分区：
文献类型：
--
作者：
de Oliveira MV;Xu G;Li B;de Souza Vespoli L;Meng X;Chen X;Yu X;de Souza SA;Intorne AC;de A Manhães AM;Musinsky AL;Koiwa H;de Souza Filho GA;Shan L;He P
精确控制细胞死亡对所有生物体的生存至关重要。拟南芥油菜素类固醇不敏感1相关受体蛋白1(BAK1)和体细胞胚胎发生受体蛋白4(SERK4)通过难以捉摸的机制冗余地负向调节细胞死亡。通过在拟南芥基因敲除集合上部署病毒诱导的BAK1/SERK4基因沉默所触发的细胞死亡抑制因子的遗传筛选，我们确定参与N-糖基化修饰的蛋白STT3a是BAK1/SERK4细胞死亡的重要调节蛋白。对糖基化途径和内质网质量控制(ERQC)成分的系统研究揭示了BAK1/SERK4及其相互作用蛋白BIR1调控细胞死亡的不同和重叠的机制。全基因组转录分析显示，在bak1/serk4突变体中，富含半胱氨酸的受体样激酶(CRK)基因成员被激活。CRK4异位表达诱导拟南芥和烟草STT3a/N糖基化依赖性细胞死亡。因此，N-糖基化和特定的ERQC组分是激活BAK1/SERK4细胞死亡所必需的，而CRK4可能是参与BAK1/SERK4调控的细胞死亡的糖基化蛋白的客户蛋白之一。
Precise control of cell death is essential for the survival of all organisms. Arabidopsis thaliana BRASSINOSTEROID INSENSITIVE 1-associated receptor kinase 1 (BAK1) and somatic embryogenesis receptor kinase 4 (SERK4) redundantly and negatively regulate cell death through elusive mechanisms. By deploying a genetic screen for suppressors of cell death triggered by virus-induced gene silencing of BAK1/SERK4 on Arabidopsis knockout collections, we identified STT3a, a protein involved in N-glycosylation modification, as an important regulator of bak1/serk4 cell death. Systematic investigation of glycosylation pathway and endoplasmic reticulum (ER) quality control (ERQC) components revealed distinct and overlapping mechanisms of cell death regulated by BAK1/SERK4 and their interacting protein BIR1. Genomewide transcriptional analysis revealed the activation of members of cysteine-rich receptor-like kinase (CRK) genes in the bak1/serk4 mutant. Ectopic expression of CRK4 induced STT3a/N-glycosylation-dependent cell death in Arabidopsis and Nicotiana benthamiana. Therefore, N-glycosylation and specific ERQC components are essential to activate bak1/serk4 cell death, and CRK4 is likely to be among client proteins of protein glycosylation involved in BAK1/SERK4-regulated cell death.
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DOI：
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发表时间：
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