Nie Yaqing, Li Yan, Yuan Penglai, Wu Chengyun, Wang Xiaoqing, Wang Chunfei, Xu Xiumei, Shen Zhenguo, Hu Zhubing
College of Life Sciences, Nanjing Agricultural University, Nanjing 210095, China.
State Key Laboratory of Crop Stress Adaptation and Improvement, School of Life Sciences, Henan University, Kaifeng 475004, China.
Plant Cell Physiol. 2024 Dec 6;65(11):1849-1861. doi: 10.1093/pcp/pcae108.
In Arabidopsis, RNA editing alters more than 500 cytidines (C) to uridines (U) in mitochondrial transcripts, a process involving the family of pentatricopeptide repeat (PPR) proteins. Here, we report a previously uncharacterized mitochondrial PLS-type PPR protein, GEND2, which functions in the mitochondrial RNA editing. The T-DNA insertion in the 5'-untranslated region of GEND2, referred to as gend2-1, results in defective root development compared to wild-type (WT) plants. A comprehensive examination of mitochondrial RNA-editing sites revealed a significant reduction in the gend2-1 mutant compared to WT plants, affecting six specific mitochondrial RNA editing sites, notably within the mitochondrial genes CcmFn-1, RPSL2 and ORFX. These genes encode critical components of cytochrome protein maturation pathway, mitochondrial ribosomal subunit and twin arginine translocation subunits, respectively. Further analysis of the transcriptional profile of the gend2-1 mutant and WT revealed a striking induction of expression in a cluster of genes associated with mitochondrial dysfunction and regulated by ANAC017, a key regulator coordinating organelle functions and stress responses. Intriguingly, the gend2-1 mutation activated an ANAC017-dependent signaling aimed at countering cell wall damage induced by cellulose synthase inhibitors, as well as an ANAC017-independent pathway that retarded root growth under normal condition. Collectively, our findings identify a novel mitochondrial PLS-type PPR protein GEND2, which participates in the editing of six specific mitochondrial RNA editing sites. Furthermore, the gend2-1 mutation triggers two distinct pathways in plants: an ANAC017-dependent pathway and ANAC017-independent pathway.
在拟南芥中，RNA编辑可将线粒体转录本中的500多个胞嘧啶（C）改变为尿嘧啶（U），这一过程涉及到五肽重复序列（PPR）蛋白家族。在此，我们报道了一种以前未被表征的线粒体PLS型PPR蛋白GEND2，它在线粒体RNA编辑中发挥作用。与野生型（WT）植物相比，GEND2的5'非翻译区的T-DNA插入（称为gend2-1）导致根系发育缺陷。对线粒体RNA编辑位点的全面检查显示，与WT植物相比，gend2-1突变体中显著减少，影响了六个特定的线粒体RNA编辑位点，特别是在线粒体基因CcmFn-1、RPSL2和ORFX内。这些基因分别编码细胞色素蛋白成熟途径、线粒体核糖体亚基和双精氨酸转运亚基的关键成分。对gend2-1突变体和WT转录谱的进一步分析显示，与线粒体功能障碍相关且受ANAC017调控的一组基因的表达显著上调，ANAC017是协调细胞器功能和应激反应的关键调节因子。有趣的是，gend2-1突变激活了一条ANAC017依赖的信号通路，旨在对抗纤维素合酶抑制剂诱导的细胞壁损伤，以及一条在正常条件下抑制根系生长的ANAC017非依赖途径。总的来说，我们的研究结果鉴定了一种新型的线粒体PLS型PPR蛋白GEND2，它参与了六个特定线粒体RNA编辑位点的编辑。此外，gend2-1突变在植物中触发了两条不同的途径：一条ANAC017依赖途径和一条ANAC017非依赖途径。
