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首页> 外文期刊>Plant Physiology >Coordination of Plastid Protein Import and Nuclear Gene Expression by Plastid-to-Nucleus Retrograde Signaling
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Coordination of Plastid Protein Import and Nuclear Gene Expression by Plastid-to-Nucleus Retrograde Signaling

机译:质体向核逆行信号介导的质体蛋白导入和核基因表达的协调。

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摘要

Expression of nuclear-encoded plastid proteins and import of those proteins into plastids are indispensable for plastid biogenesis. One possible cellular mechanism that coordinates these two essential processes is retrograde signaling from plastids to the nucleus. However, the molecular details of how this signaling occurs remain elusive. Using the plastid protein import2 mutant of Arabidopsis (Arabidopsis thaliana), which lacks the atToc159 protein import receptor, we demonstrate that the expression of photosynthesis-related nuclear genes is tightly coordinated with their import into plastids. Down-regulation of photosynthesis-related nuclear genes is also observed in mutants lacking other components of the plastid protein import apparatus. Genetic studies indicate that the coordination of plastid protein import and nuclear gene expression is independent of proposed plastid signaling pathways such as the accumulation of Mg-protoporphyrin IX and the activity of ABA INSENSITIVE4 (ABI4). Instead, it may involve GUN1 and the transcription factor AtGLK. The expression level of AtGLK1 is tightly correlated with the expression of photosynthesis-related nuclear genes in mutants defective in plastid protein import. Furthermore, the activity of GUN1 appears to down-regulate the expression of AtGLK1 when plastids are dysfunctional. Based on these data, we suggest that defects in plastid protein import generate a signal that represses photosynthesis-related nuclear genes through repression of AtGLK1 expression but not through activation of ABI4.
机译:表达核编码的质体蛋白并将这些蛋白导入质体对于质体生物发生是必不可少的。协调这两个基本过程的一种可能的细胞机制是从质体到细胞核的逆行信号传导。但是,该信号如何发生的分子细节仍然难以捉摸。使用缺少atToc159蛋白输入受体的拟南芥(Arabidopsis thaliana)质体蛋白import2突变体,我们证明了与光合作用相关的核基因的表达与其导入质体中紧密相关。在缺乏质体蛋白输入装置其他成分的突变体中,也观察到光合作用相关核基因的下调。遗传研究表明,质体蛋白输入和核基因表达的协调与拟议的质体信号传导途径无关,例如Mg-原卟啉IX的积累和ABA INSENSITIVE4(ABI4)的活性。相反,它可能涉及GUN1和转录因子AtGLK。在质体蛋白输入缺陷的突变体中,AtGLK1的表达水平与光合作用相关的核基因的表达紧密相关。此外,当质体功能异常时,GUN1的活性似乎下调了AtGLK1的表达。基于这些数据,我们建议质体蛋白输入中的缺陷产生一个信号,该信号通过抑制AtGLK1表达而不是通过激活ABI4来抑制与光合作用相关的核基因。

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  • 来源
    《Plant Physiology》 |2009年第3期|p.1339-1353|共15页
  • 作者单位

    The 21st Century Centers of Excellence Program, Cryobiofrontier Research Center, Iwate University, Morioka, Iwate 020–8550, Japan (T.K., K.N., T.I.);

    Iwate Biotechnology Research Center, Kitakami, Iwate 024–0003, Japan (H.M., R.T.);

    and Department of Environmental Biology, Faculty of Bioscience, Nagahama Institute of Bioscience and Technology, Nagahama, Shiga 526–0829, Japan (F.-S.C.);

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