AtPPR2, an Arabidopsis pentatricopeptide repeat protein, binds to plastid 23S rRNA and plays an important role in the first mitotic division during gametogenesis and in cell proliferation during embryogenesis.
AtPPR2, an Arabidopsis pentatricopeptide repeat protein, binds to plastid 23S rRNA and plays an important role in the first mitotic division during gametogenesis and in cell proliferation during embryogenesis.
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DOI：
10.1111/j.1365-313x.2011.04569.x
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发表时间：
2011-07
期刊：
影响因子：
--
通讯作者：
Xia Y
中科院分区：
文献类型：
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作者：
Lu Y;Li C;Wang H;Chen H;Berg H;Xia Y
五肽重复序列(PPR)蛋白主要参与调控包括叶绿体在内的线粒体和叶绿体的转录后过程。拟南芥PPR2基因的突变此前已被发现会导致种子发育缺陷，并减少通过雄配子体和雌配子体的传播。然而，AtPPR2的确切功能还没有定义。我们发现，AtPPR2的功能缺失突变会导致在男性和女性配子发生过程中第一次有丝分裂的停止。此外，Atppr2突变会导致胚胎发育延迟，导致胚胎死亡。Emb2750的突变似乎是AtPPR2基因座的一个微弱的突变等位基因，也会导致种子缺陷。但多数emb2750种子能萌发，但子叶白化，经常变形，萌发后幼苗生长受阻。AtPPR2主要在经历细胞分裂的植物部位表达，AtPPR2蛋白定位于叶绿体。RNA免疫沉淀和蛋白质凝胶迁移率改变分析表明，AtPPR2与质体23S rRNA结合。我们的研究增加了越来越多的证据，证明叶绿体和/或叶绿体在细胞分裂中发挥关键作用。AtPPR2可能通过调节翻译过程来微调质体功能，从而调节细胞分裂。
Pentatricopeptide repeat (PPR) proteins are mainly involved in regulating post-transcriptional processes in mitochondria and plastids, including chloroplasts. Mutations in the Arabidopsis PPR2 gene have previously been found to cause defects in seed development and reduced transmission through male and female gametophytes. However, the exact function of AtPPR2 has not been defined. We found that a loss-of-function mutation of AtPPR2 leads to arrest of the first mitotic division during both male and female gametogenesis. In addition, the Atppr2 mutation causes delayed embryogenesis, leading to embryonic lethality. Mutation in emb2750, which appears to be a weak mutant allele of the AtPPR2 locus, also results in defective seeds. However, a majority of emb2750 seeds were able to germinate, but their cotyledons were albino and often deformed, and growth of the emb2750 seedlings were arrested after germination. AtPPR2 is mainly expressed in plant parts that undergo cell division, and AtPPR2 protein was localized to chloroplasts. RNA immunoprecipitation and protein gel mobility shift assays showed that AtPPR2 binds to plastid 23S rRNA. Our study adds to a growing body of evidence that plastids and/or chloroplasts play a key role in cell division. AtPPR2 may modulate the translational process to fine-tune plastid function, thereby regulating cell division.