Mutations in SUPPRESSOR OF VARIEGATION1, a Factor Required for Normal Chloroplast Translation, Suppress var2-Mediated Leaf Variegation in Arabidopsis[W]
Mutations in SUPPRESSOR OF VARIEGATION1, a Factor Required for Normal Chloroplast Translation, Suppress var2-Mediated Leaf Variegation in Arabidopsis[W]
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DOI：
10.1105/tpc.107.054965
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发表时间：
2008-07
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影响因子：
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通讯作者：
Fei Yu;Xiayan Liu;M. Alsheikh;Sungsoon Park;S. Rodermel
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文献类型：
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作者：
Fei Yu;Xiayan Liu;M. Alsheikh;Sungsoon Park;S. Rodermel
拟南芥黄色杂色2(Var2)突变体由于缺乏叶绿体FtsH样金属蛋白酶(FtsH2/VAR2)而杂化。我们已经产生了VAR2变异的抑制因子，以深入了解在叶绿体生物发生过程中与VAR2相互作用的因素和途径。在这里，我们描述两个这样的抑制者。第一个品系Tag-Fn的杂色抑制是由于假尿苷(Ψ)合酶的叶绿体定位同源物的核基因(VARIEGATION1Svr1[Svr1])的中断引起的，该合酶在非编码RNA中将尿苷异构化为Ψ。Svr1单一突变体对var2呈上位性，表现为叶绿体rRNA加工缺陷、叶绿体翻译减少、叶绿体蛋白积累减少和叶绿体mRNA水平升高的表型综合征。在第二个品系(Tag-IE)中，杂色的抑制是由叶绿体ClpP/R蛋白酶的ClpR1亚单位基因SVR2的损伤引起的。与svr1类似，svr2对var2具有上位性，而clpr1突变体的表型与svr1相似。我们认为，TAG-FN和TAG-IE中叶绿体翻译的障碍降低了叶绿体生物发生过程中对VAR2活性的需求，从而导致了VAR2变异的抑制。与这一假设一致的是，var2的变异被叶绿体翻译的化学抑制剂抑制。在植物诱变实验中发现，SVR1不仅在尿苷异构化中起作用，而且它的物理存在是正确处理叶绿体rRNA所必需的。我们的数据表明，叶绿体rRNA加工缺陷是一种常见的，但不是普遍的，与var2变异抑制相关的分子表型。
The Arabidopsis thaliana yellow variegated2 (var2) mutant is variegated due to lack of a chloroplast FtsH-like metalloprotease (FtsH2/VAR2). We have generated suppressors of var2 variegation to gain insight into factors and pathways that interact with VAR2 during chloroplast biogenesis. Here, we describe two such suppressors. Suppression of variegation in the first line, TAG-FN, was caused by disruption of the nuclear gene (SUPPRESSOR OF VARIEGATION1 [SVR1]) for a chloroplast-localized homolog of pseudouridine (Ψ) synthase, which isomerizes uridine to Ψ in noncoding RNAs. svr1 single mutants were epistatic to var2, and they displayed a phenotypic syndrome that included defects in chloroplast rRNA processing, reduced chloroplast translation, reduced chloroplast protein accumulation, and elevated chloroplast mRNA levels. In the second line (TAG-IE), suppression of variegation was caused by a lesion in SVR2, the gene for the ClpR1 subunit of the chloroplast ClpP/R protease. Like svr1, svr2 was epistatic to var2, and clpR1 mutants had a phenotype that resembled svr1. We propose that an impairment of chloroplast translation in TAG-FN and TAG-IE decreased the demand for VAR2 activity during chloroplast biogenesis and that this resulted in the suppression of var2 variegation. Consistent with this hypothesis, var2 variegation was repressed by chemical inhibitors of chloroplast translation. In planta mutagenesis revealed that SVR1 not only played a role in uridine isomerization but that its physical presence was necessary for proper chloroplast rRNA processing. Our data indicate that defects in chloroplast rRNA processing are a common, but not universal, molecular phenotype associated with suppression of var2 variegation.