Mutation of HPR1 encoding a component of the THO/TREX complex reduces STOP1 accumulation and aluminium resistance in Arabidopsis thaliana
Mutation of HPR1 encoding a component of the THO/TREX complex reduces STOP1 accumulation and aluminium resistance in Arabidopsis thaliana
复制标题
编码 THO/TREX 复合体成分的 HPR1 突变降低了拟南芥中 STOP1 的积累和铝抗性
DOI：
10.1111/nph.16658
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发表时间：
2020-06-11
期刊：
影响因子：
9.4
通讯作者：
Huang, Chao-Feng
中科院分区：
文献类型：
--
作者：
Guo, Jinliang;Zhang, Yang;Huang, Chao-Feng
c2h2型锌指转录因子对质子根毒性敏感1 （STOP1）在拟南芥抗铝过程中发挥重要作用，通过调控包括苹果酸转运蛋白编码基因a在内的一系列抗铝基因的表达。铝激活苹果酸转运蛋白1（AtALMT1）是铝抗性的关键。stop1可能在转录后和/或翻译后水平受到Al的调控。然而，潜在的分子机制仍有待证实。我们对一个含有theatalmt1启动子驱动的荧光素酶报告基因（pAtALMT1:LUC）的甲基磺酸乙酯诱变群体进行了正向遗传筛选，并鉴定出编码THO/TREX复合物亚基的超重组蛋白1（HPR1）。我们研究了HPR1突变对铝抗性基因表达和铝抗性的影响，并研究了HPR1在stop1基因核信使RNA （mRNA）和蛋白积累中的调控作用。hpr1的突变降低了stop1调控基因的表达和相关的铝抗性。hpr1突变增加了细胞核中estop1mrna的保留，从而降低了STOP1蛋白的丰度。在hpr1突变背景下，介导STOP1降解的AtALMT1表达1（RAE1）调控突变可以部分挽救hpr1突变体的缺陷表型。我们的研究结果表明，HPR1部分通过调节核质stop1mrna的输出来调节Al抗性。
C2H2-type zinc finger transcription factor sensitive to proton rhizotoxicity 1 (STOP1) plays an essential role in aluminium (Al) resistance inArabidopsis thalianaby controlling the expression of a set of Al-resistance genes, including the malate transporter-encoding geneA. thaliana aluminium activated malate transporter 1(AtALMT1) that is critically required for Al resistance.STOP1is suggested to be modulated by Al at post-transcriptional and/or post-translational levels. However, the underlying molecular mechanisms remain to be demonstrated. We carried out a forward genetic screen on an ethyl methanesulphonate mutagenized population, which contains theAtALMT1promoter-driven luciferase reporter gene (pAtALMT1:LUC), and identifiedhyperrecombination protein 1(HPR1), which encodes a subunit of the THO/TREX complex. We investigate the effect ofhpr1mutations on the expression of Al-resistance genes and Al resistance, and we also examined the regulatory role of HPR1 in nuclear messenger RNA (mRNA) and protein accumulation ofSTOP1gene. Mutation ofHPR1reduces the expression of STOP1-regulated genes and the associated Al resistance. Thehpr1mutations increaseSTOP1mRNA retention in the nucleus and consequently decrease STOP1 protein abundance. Mutation ofregulation of AtALMT1 expression 1(RAE1) that mediates STOP1 degradation in thehpr1mutant background can partially rescue the deficient phenotypes ofhpr1mutants. Our results demonstrate that HPR1 modulates Al resistance partly through the regulation of nucleocytoplasmicSTOP1mRNA export.