ABSTRACT
The mitochondrion is a semi-autonomous organelle that provides energy for cell activities through oxidative phosphorylation. In this study, we identified a defective kernel 66 (dek66)-mutant maize with defective kernels. We characterized a candidate gene, DEK66, encoding a ribosomal assembly factor located in mitochondria and possessing GTPase activity (which belongs to the ribosome biogenesis GTPase A family). In the dek66 mutant, impairment of mitochondrial structure and function led to the accumulation of reactive oxygen species and promoted programmed cell death in endosperm cells. Furthermore, the transcript levels of most of the key genes associated with nutrient storage, mitochondrial respiratory chain complex, and mitochondrial ribosomes in the dek66 mutant were significantly altered. Collectively, the results suggest that DEK66 is essential for the development of maize kernels by affecting mitochondrial function. This study provides a reference for understanding the impact of a mitochondrial ribosomal assembly factor in maize kernel development.
Subject(s)
Plant Proteins , Zea mays , Plant Proteins/genetics , Plant Proteins/metabolism , Zea mays/metabolism , GTP Phosphohydrolases/genetics , GTP Phosphohydrolases/metabolism , Endosperm/metabolism , Mitochondria/genetics , Mitochondria/metabolism , Gene Expression Regulation, PlantABSTRACT
MAIN CONCLUSION: Arabidopsis AtPRP17, a homolog of yeast splicing factor gene PRP17, is expressed in siliques and embryos and functions in embryo development via regulating embryonic patterning. Yeast splicing factor PRP17/CDC40 is essential for cell growth through involvement in cell cycle regulation. Arabidopsis genome encodes a homolog of PRP17, AtPRP17; however, its function in Arabidopsis development is unknown. This study showed that AtPRP17 was highly expressed in siliques and embryos, and the protein was localized in the nucleus. The loss-of-function mutation of AtPRP17 led to shrunken seeds in Arabidopsis mature siliques. Further analysis revealed that the defective mature seeds of the mutant resulted from abnormal embryos with shriveled cotyledons, unequal cotyledons, swollen and shortened hypocotyls, or shortened radicles. During embryogenesis, mutant embryos showed delayed development and defective patterning of the apical and base domains, such as inhibited cotyledons and disorganized quiescent center cells and columella. Our results suggested that AtPRP17 functions in Arabidopsis embryo development via regulating embryonic patterning.
