Molecular Characterization of empty pericarp5 in Maize

Seed development is a critical stage in the life cycle of flowering plants. Understanding the mechanism governing this process is both a fundamental question in plant biology and also an important task in agriculture application as seeds are staple food and seed quality and size are controlled by the genes governing seed development process. Maize as a typical monocot plant, is also an excellent model system for monocot seed development research.;In flowering plants, RNA editing is a post-transcriptional mechanism that converts specific cytidines to uridines in both mitochondrial and plastidial transcripts, altering the genetic information encoded by these genes. It is important for posttranscriptional regulation and in some cases critical to the functions of the encoded proteins. For example, editing can restore a conserved amino acid codon, create an initiation or stop codon, or remove a stop codon that leads to a functional larger protein. Therefore, deficiency in editing may result in a compromised or complete loss of function for the encoded proteins, leading to a severe consequence in plant growth and development.;In this study, we report the molecular characterization of the empty pericarp 5 (emp5) mutant in maize ( Zea mays). Null mutation of Emp5 results in abortion of embryo and endosperm development at early stages. Emp5 encodes a mitochondrion targeted DYW-subgroup PPR protein. Analysis of the mitochondrial transcripts reveals that loss of the EMP5 function abolishes the C-to-U editing of rpl16-458 (100% edited in the wildtype), decreases the editing at nine sites in nad9, cox3 and rps12, and surprisingly increases the editing at five sites of atp6, nad1, cob and rpl16. EMP5 lacking the E+ and DYW domain still retains the substrate specificity and editing function, only at reduced efficiency. This suggests that the E+ and DYW domains of EMP5 are not essential to the EMP5 editing function, but necessary for efficiency. Analysis of the ortholog in rice indicates that OsEMP5 has a conserved function in C-to-U editing of the rice mitochondrial rpl16-458 site. Knock-down expression of OsEmp5 results in slow growth seedlings and defective seeds. These results demonstrate that EMP5 encodes a PPR-DYW protein that is required for the editing of multiple transcripts in mitochondria and the editing events, particularly the C-to-U editing at the rpl16 -458 site, are critical to the mitochondrial functions and hence to seed development in maize.