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Genetic Interactions Between BOB1 and Multiple 26S Proteasome Subunits Suggest a Role for Proteostasis in Regulating Arabidopsis Development

机译:BOB1和多个26S蛋白酶体亚基之间的遗传相互作用表明蛋白稳态在调节拟南芥发育中的作用。

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摘要

Protein folding and degradation are both required for protein quality control, an essential cellular activity that underlies normal growth and development. We investigated how BOB1, an Arabidopsis thaliana small heat shock protein, maintains normal plant development. bob1 mutants exhibit organ polarity defects and have expanded domains of KNOX gene expression. Some of these phenotypes are ecotype specific suggesting that other genes function to modify them. Using a genetic approach we identified an interaction between BOB1 and FIL, a gene required for abaxial organ identity. We also performed an EMS enhancer screen using the bob1-3 allele to identify pathways that are sensitized by a loss of BOB1 function. This screen identified genetic, but not physical, interactions between BOB1 and the proteasome subunit RPT2a. Two other proteasome subunits, RPN1a and RPN8a, also interact genetically with BOB1. Both BOB1 and the BOB1-interacting proteasome subunits had previously been shown to interact genetically with the transcriptional enhancers AS1 and AS2, genes known to regulate both organ polarity and KNOX gene expression. Our results suggest a model in which BOB1 mediated protein folding and proteasome mediated protein degradation form a functional proteostasis module required for ensuring normal plant development.
机译:蛋白质质量控​​制需要蛋白质折叠和降解,蛋白质质量控​​制是构成正常生长和发育的基础细胞活性。我们研究了拟南芥小热激蛋白BOB1如何维持正常的植物发育。 bob1突变体表现出器官极性缺陷,并具有扩大的KNOX基因表达域。这些表型中的一些是生态型特异的,表明其他基因起作用来修饰它们。使用遗传方法,我们确定了BOB1和FIL之间的相互作用,而FIL是背轴器官识别所需的基因。我们还使用bob1-3等位基因进行了EMS增强子筛选,以鉴定因BOB1功能丧失而致敏的途径。此屏幕确定了BOB1和蛋白酶体亚基RPT2a之间的遗传相互作用,但不是物理相互作用。另外两个蛋白酶体亚基RPN1a和RPN8a也与BOB1遗传相互作用。先前已证明,与BOB1和BOB1相互作用的蛋白酶体亚基都与转录增强子AS1和AS2发生遗传相互作用,后者是已知可调节器官极性和KNOX基因表达的基因。我们的结果提出了一个模型,其中 BOB1 介导的蛋白质折叠和蛋白酶体介导的蛋白质降解形成了确保正常植物发育所需的功能性蛋白稳态模块。

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