Singlet oxygen-induced signalling depends on the metabolic status of the Chlamydomonas cell

Singlet oxygen-induced signalling depends on the metabolic status of the Chlamydomonas cell
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单线态氧诱导的信号传导取决于衣藻细胞的代谢状态

DOI:
10.1101/2021.11.03.467076
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发表时间:
2021
期刊:
bioRxiv
影响因子:
--
通讯作者:
Brzezowski
Brzezowski
中科院分区:
--
文献类型:
--
作者:
Al Youssef;Saint-Sorny;Johnson;Brzezowski

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利用一种新的突变体筛选,我们鉴定出TREHALOSE 6-PHOSPHATE PHOSPHATASE 1 (TSPP1)是一种将海藻糖6-PHOSPHATE (Tre6P)去磷酸化为reinhardtii chlamydomonas海藻糖的功能性酶。tspp1敲除通过显著改变转录组导致细胞代谢重编程。作为次要效应,tspp1在o2诱导的叶绿体逆行信号传导中也表现出损伤。从转录组学分析和代谢物分析中,我们得出结论,某些代谢物的积累或缺乏直接影响o2信号传导。o2诱导的leglutathione过氧化物酶5(GPX5)基因表达受线粒体中三羧酸循环(TCA循环)和细胞质中二羧酸代谢的中间体富马酸盐含量增加的抑制,而另一种TCA循环中间体乌头酸促进GPX5基因表达。此外,在tspp1突变体中,编码叶绿体到细胞核信号传导重要成分的基因PSBP2、MBS和SAK1的转录水平下降,这可以通过外源施用乌头碱来恢复。我们证明了叶绿体逆行信号涉及的1o2依赖于线粒体和细胞质过程,细胞的代谢状态决定了对1o2的反应。
Using a novel mutant screen, we identified TREHALOSE 6-PHOSPHATE PHOSPHATASE 1 (TSPP1) as a functional enzyme dephosphorylating trehalose 6-phosphate (Tre6P) to trehalose inChlamydomonas reinhardtii. Thetspp1knock-out results in reprogramming of the cell metabolism via significantly altered transcriptome. As a secondary effect,tspp1also shows impairment in1O2-induced chloroplast retrograde signalling. From transcriptomic analysis and metabolite profiling, we conclude that accumulation or deficiency of certain metabolites directly affect1O2-signalling.1O2-inducibleGLUTATHIONE PEROXIDASE 5(GPX5) gene expression is suppressed by increased content of fumarate, an intermediate in the tricarboxylic acid cycle (TCA cycle) in mitochondria and dicarboxylate metabolism in the cytosol, while it is promoted by another TCA cycle intermediate, aconitate. Furthermore, genes encoding known essential components of chloroplast-to-nucleus1O2-signalling, PSBP2, MBS, and SAK1, show decreased transcript levels in thetspp1mutant, which can be rescued by exogenous application of aconitate. We demonstrate that chloroplast retrograde signalling involving1O2depends on mitochondrial and cytosolic processes and that the metabolic status of the cell determines the response to1O2.
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