Date: Sunday, January 15, 2012
Time: 10:40 AM
Time: 10:40 AM
Room: Pacific Salon 6-7 (2nd Floor)
Nuclear genes are essential for expression of the mitochondrial genome and for the function of mitochondrial protein complexes. Interaction of the plant mitochondrial and nuclear genetic systems is exemplified by mitochondrial-encoded cytoplasmic male sterility (CMS) under the control of nuclear fertility restoration (restorer) genes. Most restorer genes cloned to date encode pentatricopeptide repeat (PPR) proteins that regulate post-transcriptional expression of mitochondrial CMS genes. Restorer PPR genes have evolved specificity for CMS gene silencing, in contrast to the majority of PPR genes with functions central to organelle gene expression. The CMS-S system of maize is characterized by a pollen collapse phenotype, and by numerous restorer mutations that rescue pollen function but condition homozygous-lethal seed phenotypes. A collection of restorer mutants was recovered from Mutator (Mu) transposon-active, CMS-S lines. Profiling of mitochondrial proteins and transcripts in pollen from normal-cytoplasm and restored CMS-S plants associated several non-allelic mutants with post-transcriptional failure to accumulate mitochondrial-encoded respiratory subunits. Illumina sequencing of Mu-flanking regions demonstrated the co-segregation of one restorer mutation with a Mu insertion in a gene encoding the mitochondrial-targeted ribosomal protein L6. Restorer mutations therefore can rescue CMS-S pollen by disrupting central features of mitochondrial gene expression that are expendable in pollen but essential for seed development. CMS-S fertility restoration affords a novel genetic approach that can be used to investigate the nuclear regulation of mitochondrial biogenesis and function in plants.