Maize Defective Kernel605 Encodes a Canonical DYW-Type PPR Protein That Edits a Conserved Site of nad1 and Is Essential for Seed Nutritional Quality.

Pentatricopeptide repeat (PPR) proteins involved in mitochondrial RNA cytidines (C) to uridines (U) editing mostly result in the stagnant embryo and endosperm development when losing function. However, less is known about PPR that 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, complex III and IV in the cytochrome pathway, as well as AOX2 in the alternative respiratory pathway, are dramatically increased. Interestingly, the mutation resulted in opaque endosperm and increased levels of the free amino acids ALA, ASP and PHE in dek605. The down- and up-regulated genes were mainly involving in stress response-related and seed dormancy-related pathways, respectively, were observed after transcriptome analysis of dek605 at 12 day after pollination (DAP). 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.