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The expression systems of the mitochondrial genes are derived from their bacterial ancestors, but have evolved many new features in their eukaryotic hosts. Mitochondrial RNA splicing is a complex process regulated by families of nucleus-encoded RNA-binding proteins, few of which have been characterized in maize (Zea mays L.). Here, we identified the Zea mays small kernel 3 (Zmsmk3) candidate gene, which encodes a mitochondrial transcription termination factor (mTERF) containing two mTERF motifs, which is conserved in monocotyledon; and the target introns were also quite conserved during evolution between monocotyledons and dicotyledons. The mutations of Zmsmk3 led to arrested embryo and endosperm development, resulting in small kernels. A transcriptome of 12 days after pollination endosperm analysis revealed that the starch biosynthetic pathway and the zein gene family were downregulated in the Zmsmk3 mutant kernels. ZmSMK3 is localized in mitochondria. The reduced expression of ZmSmk3 in the mutant resulted in the splicing deficiency of mitochondrial nad4 intron1 and nad1 intron4, causing a reduction in complex I assembly and activity, impairing mitochondria structure and activating the alternative respiratory pathway. So, the results suggest that ZmSMK3 is required for the splicing of nad4 intron 1 and nad1 intron 4, complex I assembly and kernel development in maize. [ABSTRACT FROM AUTHOR]

Group II introns are common in the mitochondrial genome of higher plant species. The splicing of these introns is a complex process involving the synergistic action of multiple factors. However, few of these factors have been characterized in maize. In this study, we found that the Empty pericarp11 (Emp11) gene, which encodes a P-type pentatricopeptide repeat (PPR) protein, is required for the development of maize seeds. The loss of Emp11 function seriously impairs embryo and endosperm development, resulting in empty pericarp seeds in maize, and alteration in Emp11 expression leads to quantitative variation in kernel size and weight. We found that the emp11 mutants showed a failure in nad1 intron splicing, exhibited a severe reduction in complex I assembly and activity, mitochondrial structure disturbances, and an increase in alternative oxidase AOX2 and AOX3 levels. Interestingly, the emp11 phenotype was very severe in the W22 inbred line but could be partially recovered in B73 BC2F2 segregating ears. These results suggest that EMP11 serves as a factor for the splicing of mitochondrial nad1 introns and is required for mitochondrial function to ensure proper seed development in maize. [ABSTRACT FROM AUTHOR]