摘要

In flowering plants, many respiration-related proteins are encoded by the mitochondrial genome and the splicing of mitochondrion-encoded messenger RNA (mRNA) involves a complex collaboration with nuclear-encoded proteins. Pentatricopeptide repeat (PPR) proteins have been implicated in these RNA-protein interactions. Maize defective kernel 2 (dek2) is a classic mutant with small kernels and delayed development. Through positional cloning and allelic confirmation, we found Dek2 encodes a novel P-type PPR protein that targets mitochondria. Mitochondrial transcript analysis indicated that dek2 mutation causes reduced splicing efficiency of mitochondrial nad1 intron 1. Mitochondrial complex analysis in dek2 immature kernels showed severe deficiency of complex I assembly. Dramatically up-regulated expression of alternative oxidases (AOXs), transcriptome data, and TEM analysis results revealed that proper splicing of nad1 is critical for mitochondrial functions and inner cristaes morphology. This study indicated that Dek2 is a new PPR protein that affects the splicing of mitochondrial nad1 intron 1 and is required for mitochondrial function and kernel development.