Maize Dek37 Encodes a P-type PPR Protein That Affects cis-Splicing of Mitochondrial nad2 Intron 1 and Seed Development

Abstract

Abstract Mitochondrial group II introns require the participation of numerous nucleus-encoded general and specific factors to achieve efficient splicing in vivo. Pentatricopeptide repeat (PPR) proteins have been implicated in assisting group II intron splicing. Here, we identified and characterized a new maize seed mutant, defective kernel 37 (dek37), which has significantly delayed endosperm and embryo development. Dek37 encodes a classic P-type PPR protein that targets mitochondria. The dek37 mutation causes no detectable DEK37 protein in mutant seeds. Mitochondrial transcripts analysis indicated that dek37 mutation decreases splicing efficiency of mitochondrial nad2 intron 1, leading to reduced assembly and NADH dehydrogenase activity of complex I. Transmission Electron Microscopy (TEM) revealed severe morphological defects of mitochondria in dek37. Transcriptome analysis of dek37 endosperm indicated enhanced expression in the alternative respiratory pathway and extensive differentially expressed genes related to mitochondrial function. These results indicated that Dek37 is involved in cis-splicing of mitochondrial nad2 intron 1 and is required for complex I assembly, mitochondrial function, and seed development in maize.