Abstract

Pentatricopeptide repeat (PPR) proteins involved in mitochondrial RNA cytidine (C)-to-uridine (U) editing mostly result in stagnant embryo and endosperm development upon loss of function. However, less is known about PPRs that are involved in farinaceous endosperm formation and maize quality. Here, we cloned a maize DYW-type PPR Defective Kernel605 (Dek605). Mutation of Dek605 delayed seed and seedling development. Mitochondrial transcript analysis of dek605 revealed that loss of DEK605 impaired C-to-U editing at the nad1-608 site and fails to alter Ser²⁰³ to Phe²⁰³ in NAD1 (dehydrogenase complex I), disrupting complex I assembly and reducing NADH dehydrogenase activity. Meanwhile, complexes III and IV in the cytochrome pathway, as well as AOX2 in the alternative respiratory pathway, are dramatically increased. Interestingly, the dek605 mutation resulted in opaque endosperm and increased levels of the free amino acids alanine, aspartic acid and phenylalanine. The down- and upregulated genes mainly involved in stress response-related and seed dormancy-related pathways, respectively, were observed after transcriptome analysis of dek605 at 12 d after pollination. Collectively, these results indicate that Dek605 specifically affects the single nad1-608 site and is required for normal seed development and resulted in nutritional quality relevant amino acid accumulation.

中文翻译：

---

玉米缺陷 Kernel605 编码规范 DYW 型 PPR 蛋白，该蛋白可编辑 nad1 的保守位点，并且对种子营养质量至关重要。

摘要

参与线粒体 RNA 胞苷 (C) 到尿苷 (U) 编辑的五肽重复 (PPR) 蛋白主要导致功能丧失后胚胎和胚乳发育停滞。然而，对参与粉质胚乳形成和玉米品质的 PPR 知之甚少。在这里，我们克隆了一个玉米 DYW 型 PPR Defective Kernel605 ( Dek605 )。Dek605 的突变延迟了种子和幼苗的发育。dek605 的线粒体转录本分析显示，DEK605 的缺失损害了nad1 -608 位点的C-to-U 编辑，并且未能将 Ser ²⁰³改变为 Phe ²⁰³在 NAD1（脱氢酶复合物 I）中，破坏复合物 I 组装并降低 NADH 脱氢酶活性。同时，细胞色素通路中的复合物 III 和 IV 以及替代呼吸通路中的 AOX2 显着增加。有趣的是，dek605 突变导致不透明的胚乳和游离氨基酸丙氨酸、天冬氨酸和苯丙氨酸的水平增加。在授粉后 12 d对dek605进行转录组分析后，分别观察到下调和上调基因主要参与胁迫响应相关和种子休眠相关途径。总的来说，这些结果表明Dek605特别影响单个nad1-608 位点，是正常种子发育所必需的，并导致与营养质量相关的氨基酸积累。