Pentatricopeptide repeat proteins are involved in mitochondrial both transcriptional and posttranscriptional regulation. Ppr2 is a general mitochondrial translation factor that plays a critical role in the synthesis of all mitochondrial DNA-encoded oxidative phosphorylation subunits, which are essential for mitochondrial respiration. Our previous analysis showed that deletion resulted in increased expression of iron uptake genes and caused ferroptosis-like cell death in . In the present work, we showed that deletion of reduced viability on glycerol- and galactose-containing media.Php4 is a transcription repressor that regulates iron homeostasis in fission yeast. We found that in the deletion strain, Php4 was constitutively active and accumulated in the nucleus in the stationary phase. We also found that deletion of decreased the ferroptosis-related protein Gpx1 in the mitochondria. Overexpression of Gpx1 improves the viability of Δ cells. We showed that the deletion of increased the production of ROS, downregulated heme synthesis and iron-sulfur cluster proteins, and induced stress proteins. Finally, we observed the nuclear accumulation of Pap1-GFP and Sty1-GFP, suggesting that Sty1 and Pap1 in response to cellular stress in the deletion strain. These results suggest that deletion may cause mitochondrial dysfunction, which is likely to lead to iron-sensing defect and iron starvation response, resulting in perturbation of iron homeostasis and increased hydroxyl radical production. The increased hydroxyl radical production triggers cellular responses in the deletion strain.

中文翻译：

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ppr2 的缺失会干扰粟酒裂殖酵母中的铁感应并导致氧化应激反应

五肽重复蛋白参与线粒体转录和转录后调节。 Ppr2 是一种通用线粒体翻译因子，在所有线粒体 DNA 编码的氧化磷酸化亚基的合成中发挥着关键作用，而氧化磷酸化亚基对于线粒体呼吸至关重要。我们之前的分析表明，缺失导致铁摄取基因表达增加，并导致铁死亡样细胞死亡。在目前的工作中，我们证明了在含有甘油和半乳糖的培养基上删除会降低活力。Php4 是一种转录抑制因子，可调节裂殖酵母中的铁稳态。我们发现，在缺失菌株中，Php4 具有组成型活性，并在稳定期积累在细胞核中。我们还发现，线粒体中铁死亡相关蛋白 Gpx1 的缺失减少了。 Gpx1 的过度表达可提高 Δ 细胞的活力。我们发现，缺失增加了 ROS 的产生，下调了血红素合成和铁硫簇蛋白，并诱导了应激蛋白。最后，我们观察到 Pap1-GFP 和 Sty1-GFP 的核积累，表明 Sty1 和 Pap1 在缺失菌株中响应细胞应激。这些结果表明，缺失可能导致线粒体功能障碍，这可能导致铁感应缺陷和铁饥饿反应，从而扰乱铁稳态并增加羟自由基的产生。羟基自由基产生的增加会触发缺失菌株的细胞反应。