Functional specialization amongst the Arabidopsis Toc159 family of chloroplast protein import receptors
Functional specialization amongst the Arabidopsis Toc159 family of chloroplast protein import receptors
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DOI：
10.1105/tpc.104.023309
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发表时间：
2004-08-01
期刊：
影响因子：
11.6
通讯作者：
Jarvis, P
中科院分区：
文献类型：
--
作者：
Kubis, S;Patel, R;Jarvis, P
前蛋白输入叶绿体的初始阶段是由受体 GTPase Toc159 介导的。在拟南芥中，Toc159 由一个小基因家族编码：atTOC159、atTOC132、atTOC120 和 atTOC90。系统发育分析表明，植物中至少存在两种不同的 Toc159 亚型，以 atToc159 和 atToc132/atToc120 为特征。 atTOC159 在年轻的光合组织中强烈表达，而 atTOC132 和 atTOC120 均以低水平表达，因此在非光合组织中相对突出。基于其敲除突变体的白化表型，atToc159先前被认为是对光合前蛋白具有特异性的受体。为了阐明其他亚型的作用，我们对每种亚型的拟南芥敲除突变体进行了表征。没有一个单一突变体具有强烈的可见表型，但 toc132 toc120 双纯合子似乎与 toc159 相似，表明 atToc132 和 atToc120 之间存在冗余。转基因互补研究证实了这种冗余，但显示 atToc132/atToc120 和 atToc159 或 atToc90 之间几乎没有功能重叠。与 toc159 不同，toc132 toc120 导致根质体结构异常。此外，当使用蛋白质组学和转录组学将 toc132 与 ppi1（一种在光合蛋白的表达、导入和积累方面存在特异性缺陷的受体突变体）进行比较时，观察到了重大差异，表明 atToc132（和 atToc120）对非光合蛋白具有特异性。当 atToc159 和另一种亚型的主要亚型 atToc132 均缺失时，就会产生胚胎致死表型，这证明了 Toc159 在输入机制中的重要作用。
The initial stages of preprotein import into chloroplasts are mediated by the receptor GTPase Toc159. In Arabidopsis thaliana, Toc159 is encoded by a small gene family: atTOC159, atTOC132, atTOC120, and atTOC90. Phylogenetic analysis suggested that at least two distinct Toc159 subtypes, characterized by atToc159 and atToc132/atToc120, exist in plants. atTOC159 was strongly expressed in young, photosynthetic tissues, whereas atTOC132 and atTOC120 were expressed at a uniformly low level and so were relatively prominent in nonphotosynthetic tissues. Based on the albino phenotype of its knockout mutant, atToc159 was previously proposed to be a receptor with specificity for photosynthetic preproteins. To elucidate the roles of the other isoforms, we characterized Arabidopsis knockout mutants for each one. None of the single mutants had strong visible phenotypes, but toc132 toc120 double homozygotes appeared similar to toc159, indicating redundancy between atToc132 and atToc120. Transgenic complementation studies confirmed this redundancy but revealed little functional overlap between atToc132/atToc120 and atToc159 or atToc90. Unlike toc159, toc132 toc120 caused structural abnormalities in root plastids. Furthermore, when proteomics and transcriptomics were used to compare toc132 with ppi1 (a receptor mutant that is specifically defective in the expression, import, and accumulation of photosynthetic proteins), major differences were observed, suggesting that atToc132 (and atToc120) has specificity for nonphotosynthetic proteins. When both atToc159 and the major isoform of the other subtype, atToc132, were absent, an embryo-lethal phenotype resulted, demonstrating the essential role of Toc159 in the import mechanism.