Coordination of Plastid Protein Import and Nuclear Gene Expression by Plastid-to-Nucleus Retrograde Signaling
Coordination of Plastid Protein Import and Nuclear Gene Expression by Plastid-to-Nucleus Retrograde Signaling
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DOI：
10.1104/pp.109.145987
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发表时间：
2009-11-01
期刊：
影响因子：
7.4
通讯作者：
Inaba, Takehito
中科院分区：
文献类型：
--
作者：
Kakizaki, Tomohiro;Matsumura, Hideo;Inaba, Takehito
胞核编码的胞质蛋白的表达和这些蛋白的输入对于胞质的生物发生是必不可少的。协调这两个基本过程的一个可能的细胞机制是从叶绿体到细胞核的逆行信号。然而，这种信号如何发生的分子细节仍然难以捉摸。利用缺乏atToc159蛋白输入受体的拟南芥(Arabiopsis Thaliana)叶绿体蛋白Import2突变体，我们证明了与光合作用相关的核基因的表达与它们进入叶绿体的紧密协调。在缺乏叶绿体蛋白输入装置的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。遗传学研究表明，叶绿体蛋白输入和核基因表达的协调不依赖于已提出的叶绿体信号通路，如镁原卟啉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。在叶绿体蛋白输入缺陷突变株中，AtGLK1的表达水平与光合作用相关核基因的表达密切相关。此外，当质体功能失调时，GUN1的活性似乎下调了AtGLK1的表达。基于这些数据，我们认为，叶绿体蛋白输入的缺陷产生了一个信号，该信号通过抑制AtGLK1的表达而不是激活ABI4来抑制光合作用相关的核基因。
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.