An mTERF domain protein functions in group II intron splicing in maize chloroplasts

An mTERF domain protein functions in group II intron splicing in maize chloroplasts
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DOI:
10.1093/nar/gku112
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发表时间:
2014-04-01
影响因子:
14.9
通讯作者:
Barkan, Alice
Barkan, Alice
中科院分区:
生物学2区
文献类型:
--
作者:
Hammani, Kamel;Barkan, Alice

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线粒体转录终止因子(mTERF)蛋白是一种核酸结合蛋白,其特征是类似于30个氨基酸的简并螺旋重复。后生动物基因组编码一个小的mTERF蛋白家族,其成员影响线粒体基因表达和DNA复制。高等植物的mTERF家族大约有30个成员,分布在线粒体或叶绿体中。几种mTERF蛋白对植物发育和生理的影响已被描述,但mTERF蛋白在植物中的分子功能尚不清楚。我们发现玉米mTERF蛋白Zm-mTERF4促进叶绿体中II族内含子的剪接。Zm-mTERF4与许多叶绿体内含子共免疫沉淀,即使在亚形态的Zm-mTERF4突变体中,其中一些内含子的剪接也被破坏。此外,Zm-mTERF4存在于包括已知叶绿体剪接因子在内的高分子量复合物中。两种转移RNA (trnI-GAU和trnA-UGC)和一种核糖体蛋白信使RNA (rpl2)的剪接对Zm-mTERF4的缺失特别敏感,导致Zm-mTERF4突变体中质体核糖体的缺失。这些发现将mTERF家族已知的功能库扩展到包括II组内含子剪接,并表明在叶绿体RNA剪接中的保守作用是拟南芥中Zm-mTERF4同源基因BSM/Rugosa2突变的生理缺陷的基础。
The mitochondrial transcription termination factor (mTERF) proteins are nucleic acid binding proteins characterized by degenerate helical repeats of similar to 30 amino acids. Metazoan genomes encode a small family of mTERF proteins whose members influence mitochondrial gene expression and DNA replication. The mTERF family in higher plants consists of roughly 30 members, which localize to mitochondria or chloroplasts. Effects of several mTERF proteins on plant development and physiology have been described, but molecular functions of mTERF proteins in plants are unknown. We show that a maize mTERF protein, Zm-mTERF4, promotes the splicing of group II introns in chloroplasts. Zm-mTERF4 coimmunoprecipitates with many chloroplast introns and the splicing of some of these introns is disrupted even in hypomorphic Zm-mterf4 mutants. Furthermore, Zm-mTERF4 is found in high molecular weight complexes that include known chloroplast splicing factors. The splicing of two transfer RNAs (trnI-GAU and trnA-UGC) and one ribosomal protein messenger RNA (rpl2) is particularly sensitive to the loss of Zm-mTERF4, accounting for the loss of plastid ribosomes in Zm-mTERF4 mutants. These findings extend the known functional repertoire of the mTERF family to include group II intron splicing and suggest that a conserved role in chloroplast RNA splicing underlies the physiological defects described for mutations in BSM/Rugosa2, the Zm-mTERF4 ortholog in Arabidopsis.