Conditional repression of essential chloroplast genes: Evidence for new plastid signaling pathways.
Conditional repression of essential chloroplast genes: Evidence for new plastid signaling pathways.
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DOI：
10.1016/j.bbabio.2014.11.011
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发表时间：
2015-09
期刊：
影响因子：
--
通讯作者：
J. Rochaix;S. Ramundo
中科院分区：
文献类型：
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作者：
J. Rochaix;S. Ramundo
莱茵衣藻叶绿体抑制基因表达系统的建立为研究叶绿体必需基因的作用打开了大门。该方法已被用于分析这类编码RNA聚合酶(rpoA) α亚基、核糖体蛋白（rps12）和atp依赖性ClpP蛋白酶（clpP1）催化亚基的三个叶绿体基因。这三种相应蛋白的耗竭会导致生长停滞和细胞死亡。叶绿体转录和翻译的关闭增加了一组质体转录物的丰度，这些转录物主要包括转录、翻译和蛋白质水解，并揭示了叶绿体基因回路中的多个调节反馈回路。ClpP的缺失深刻地影响质体蛋白稳态，并引发细胞广泛的细胞质空泡化的自噬样反应。它还会引发叶绿体和核基因表达的变化，导致伴侣蛋白、蛋白酶、泛素相关蛋白和参与脂质运输和类囊体生物发生的蛋白质的丰度增加。这些特征是叶绿体中未折叠蛋白反应的标志，并对质体蛋白稳态和质体信号传导提出了新的问题。这篇文章是《叶绿体生物发生》特刊的一部分。
The development of a repressible chloroplast gene expression system inChlamydomonas reinhardtiihas opened the door for studying the role of essential chloroplast genes. This approach has been used to analyze three chloroplast genes of this sort coding for the α subunit of RNA polymerase (rpoA), a ribosomal protein (rps12) and the catalytic subunit of the ATP-dependent ClpP protease (clpP1). Depletion of the three corresponding proteins leads to growth arrest and cell death. Shutdown of chloroplast transcription and translation increases the abundance of a set of plastid transcripts that includes mainly those involved in transcription, translation and proteolysis and reveals multiple regulatory feedback loops in the chloroplast gene circuitry. Depletion of ClpP profoundly affects plastid protein homeostasis and elicits an autophagy-like response with extensive cytoplasmic vacuolization of cells. It also triggers changes in chloroplast and nuclear gene expression resulting in increased abundance of chaperones, proteases, ubiquitin-related proteins and proteins involved in lipid trafficking and thylakoid biogenesis. These features are hallmarks of an unfolded protein response in the chloroplast and raise new questions on plastid protein homeostasis and plastid signaling.This article is part of a Special Issue entitled: Chloroplast Biogenesis.