RNA editing in plant mitochondria, cytoplasmic male sterility and plant breeding

Abstract

RNA editing in plant mitochondria is a post-transcriptional process involving the partial change of C residues into U. These C to U changes lead to the synthesis of proteins with an amino acid sequence different to that predicted from the gene. Proteins produced from edited mRNAs are more similar to those from organisms where this process is absent. This biochemical process involves cytidine deamination. The cytoplasmic male sterility (CMS) phenotype generated by the incompatibility between the nuclear and the mitochondrial genomes is an important agronomical trait which prevents inbreeding and favors hybrid production. The hypothesis that RNA editing leads to functional proteins has been proposed. This hypothesis was tested by constructing transgenic plants expressing a mitochondrial protein translated from unedited mRNA. The transgenic "unedited" protein was addressed to the mitochondria leading to the appearance of mitochondrial dysfunction and generating the male sterile phenotype in transgenic tobacco plants. Male sterile plants were also obtained by expressing specifically a bacterial ribonuclease in the anthers. The economical benefits of artificially engineered male-sterile plants or carrying the (native) spontaneous CMS phenotype, implies the restoration to obtain fertile hybrids that will be used in agriculture. Restoration to fertility of transgenic plants was obtained either by crossing male-sterile plants carrying the "unedited" mRNA with plants carrying the same RNA, but in the antisense orientation or, in the case of plants expresing the ribonuclease, by crossing male-sterile plants with plants expressing an inhibitor specific of this enzyme