Chloroplasts constantly experience photo‐oxidative stress while performing photosynthesis. This is particularly true under abiotic stresses that lead to the accumulation of reactive oxygen species (ROS) which oxidize DNA, proteins and lipids. Reactive oxygen species can also act as signals to induce acclimation through chloroplast degradation, cell death and nuclear gene expression. To better understand the mechanisms behind ROS signaling from chloroplasts, we have used the Arabidopsis thaliana mutant plastid ferrochelatase two (fc2) that conditionally accumulates the ROS singlet oxygen (¹O₂) leading to chloroplast degradation and eventually cell death. Here we have mapped mutations that suppress chloroplast degradation in the fc2 mutant and demonstrate that they affect two independent loci (PPR30 and mTERF9) encoding chloroplast proteins predicted to be involved in post‐transcriptional gene expression. These mutants exhibited broadly reduced chloroplast gene expression, impaired chloroplast development and reduced chloroplast stress signaling. Levels of ¹O₂, however, could be uncoupled from chloroplast degradation, suggesting that PPR30 and mTERF9 are involved in ROS signaling pathways. In the wild‐type background, ppr30 and mTERF9 mutants were also observed to be less susceptible to cell death induced by excess light stress. While broad inhibition of plastid transcription with rifampicin was also able to suppress cell death in fc2 mutants, specific reductions in plastid gene expression using other mutations was not always sufficient. Together these results suggest that plastid gene expression, or the expression of specific plastid genes by PPR30 and mTERF0, is a necessary prerequisite for chloroplasts to activate the ¹O₂ signaling pathways to induce chloroplast quality control pathways and/or cell death.

中文翻译：

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叶绿体定位的五肽重复序列蛋白30和“线粒体”转录终止因子9在叶绿体质量控制中的作用。

叶绿体在进行光合作用的过程中不断经历光氧化胁迫。在非生物胁迫下尤其如此，非生物胁迫导致氧化DNA，蛋白质和脂质的活性氧（ROS）积累。活性氧还可以通过叶绿体降解，细胞死亡和核基因表达来诱导驯化。为了更好地了解叶绿体中ROS信号背后的机制，我们使用了拟南芥突变体质体铁螯合酶2（fc2），有条件地累积ROS单线态氧（¹ O ₂）导致叶绿体降解并最终导致细胞死亡。在这里，我们绘制了可抑制fc2突变体中叶绿体降解的突变图谱，并证明它们影响了两个独立的基因座（PPR30和mTERF9），这些基因位点编码预计参与转录后基因表达的叶绿体蛋白。这些突变体表现出广泛减少的叶绿体基因表达，受损的叶绿体发育和减少的叶绿体胁迫信号。然而，¹ O _2的水平可能与叶绿体降解无关，这表明PPR30和mTERF9参与了ROS信号通路。在野生型背景下，ppr30和mTERF9还观察到突变体对过度的光胁迫诱导的细胞死亡较不敏感。尽管用利福平对质体转录的广泛抑制也能够抑制fc2突变体中的细胞死亡，但使用其他突变来特异性降低质体基因表达并不总是足够的。这些结果共同表明，质体基因表达或PPR30和mTERF0表达的特定质体基因是叶绿体激活¹ O ₂信号传导途径以诱导叶绿体质量控制途径和/或细胞死亡的必要先决条件。