Abstract
In flowering plants, C-to-U RNA editing can be critical to normal functions of mitochondrion-encoded proteins. Mitochondrial C-to-U RNA editing is facilitated by many factors from diverse protein families, of which the pentatricopeptide repeat (PPR) proteins play an important role. Owing to their large number and frequent embryo lethality in mutants, functions of many PPRs remain unknown. In this study, we characterized a mitochondrion-localized DYW-type PPR protein, DEK48, functioning in the C-to-U RNA editing at multiple mitochondrial transcripts in maize. Null mutation of Dek48 severely arrests embryo and endosperm development, causing a defective kernel (dek) phenotype, named dek48. DEK48 loss of function abolishes the C-to-U editing at nad3-185, -215, and nad4-376, -977 sites and decreases the editing at 11 other sites, resulting in the alteration of the corresponding amino acids. Consequently, the absence of editing caused reduced assembly and activity of complex I in dek48. Interestingly, we identified a point mutation in dek48-3 causing a deletion of the Tryptophan (W) residue in the DYW motif that abolishes the editing function. In sum, this study reveals the function of DEK48 in the C-to-U editing in mitochondrial transcripts and seed development in maize, and it demonstrates a critical role of the W residue in the DYW triplet motif of DEK48 for the C-to-U editing function in vivo.
Highlights
Mitochondria are highly metabolically active organelles, producing ATP for eukaryotic cell activities through the electron transport respiratory chain (ETC)
The model of DEK48 structure was predicted based on template PPR10 using Phyre2
days after pollination (DAP), the endosperm development was severely in dek48-1 bryo continued to develop, maturation stage as indicated by thedelayed differenticompared with the. These results indicate that loss of function in Dek48 ated leaf primordia (LP), shoot apical meristem (SAM), and root apical meristem (RAM)
Summary
Mitochondria are highly metabolically active organelles, producing ATP for eukaryotic cell activities through the electron transport respiratory chain (ETC). Electrons from nicotinamide adenine dinucleotide (NADH) dehydrogenase (complex I) and succinate dehydrogenase (complex II) are transported through ubiquinone and cytochrome c reductase (complex III) to cytochrome c oxidase (complex IV), generating most cellular ATP by ATP synthase (complex V) [1]. Approximately 95% of the ancestral mitochondrial genes from the α-proteobacteria were lost or transferred to host nucleus, and only 5% were retained in the mitochondrial genome [2]. The expression of these mitochondrial genes is highly regulated by numerous nucleus-encoded factors including transcription, posttranscriptional processing, and translation. A major regulatory process is RNA processing, which includes intron splicing, RNA cleavage, RNA maturation and stabilization, and RNA editing [3]
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