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首页> 外文期刊>Molecular Microbiology >Two essential FtsH proteases control the level of the Fur repressor during iron deficiency in the cyanobacterium Synechocystis sp. PCC 6803
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Two essential FtsH proteases control the level of the Fur repressor during iron deficiency in the cyanobacterium Synechocystis sp. PCC 6803

机译:在蓝藻集胞藻属中,铁缺乏时,两种必需的FtsH蛋白酶控制Fur阻遏物的水平。 PCC 6803

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Summary: The cyanobacterium Synechocystis sp. PCC 6803 expresses four different FtsH protease subunits (FtsH1-4) that assemble into specific homo- and heterocomplexes. The FtsH2/FtsH3 complex is involved in photoprotection but the physiological roles of the other complexes, notably the essential FtsH1/FtsH3 complex, remain unclear. Here we show that the FtsH1 and FtsH3 proteases are involved in the acclimation of cells to iron deficiency. A mutant conditionally depleted in FtsH3 was unable to induce normal expression of the IsiA chlorophyll-protein and FutA1 iron transporter upon iron deficiency due to a block in transcription, which is regulated by the Fur transcriptional repressor. Levels of Fur declined in the WT and the FtsH2 null mutant upon iron depletion but not in the FtsH3 downregulated strain. A similar stabilizing effect on Fur was also observed in a mutant conditionally depleted in the FtsH1 subunit. Moreover, a mutant overexpressing FtsH1 showed reduced levels of Fur and enhanced accumulation of both IsiA and FutA1 even under iron sufficiency. Analysis of GFP-tagged derivatives and biochemical fractionation supported a common location for FtsH1 and FtsH3 in the cytoplasmic membrane. Overall we propose that degradation of the Fur repressor mediated by the FtsH1/FtsH3 heterocomplex is critical for acclimation to iron depletion.
机译:摘要:蓝藻集胞藻。 PCC 6803表达四个不同的FtsH蛋白酶亚基(FtsH1-4),它们组装成特定的同型和异型复合体。 FtsH2 / FtsH3复合物参与光保护,但是其他复合物,尤其是必需的FtsH1 / FtsH3复合物的生理作用仍然不清楚。在这里,我们显示FtsH1和FtsH3蛋白酶参与细胞对铁缺乏的适应。有条件地贫化FtsH3的突变体由于缺铁而无法诱导IsiA叶绿素蛋白和FutA1铁转运蛋白的正常表达,这是由于转录受阻,由Fur转录阻遏物调控。铁减少后,WT和FtsH2无效突变体的Fur水平下降,而FtsH3下调的菌株却没有下降。在条件有限的FtsH1亚基缺失的突变体中,也观察到了对Fur的类似稳定作用。此外,即使在铁充足的条件下,过表达FtsH1的突变体也能降低Fur的水平,并增强IsiA和FutA1的积累。带有GFP标签的衍生物的分析和生化分离支持FtsH1和FtsH3在细胞质膜中的共同位置。总的来说,我们提出由FtsH1 / FtsH3杂合物介导的Fur阻遏物的降解对于适应铁耗竭至关重要。

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