Cytoplasmic Male Sterility
Cytoplasmic male sterility (cms) is a maternally inherited inability to produce functional pollen. In many cms systems, restoration of male fertility can occur in the presence of specific nuclear genes. These fertility-restorer genes are thought to block or compensate for cytoplasmic dysfunctions that are phenotypically expressed during pollen development. The male sterility associated with T cytoplasm maize is due to the action of a chimeric mitochondrial gene, T-urf13, unique to the T cytoplasm. Fertility restoration in cmsT maize requires the action of dominant alleles of two unlinked nuclear-restorer loci, rf1 and rf2. The rf2 gene encodes a mitochondrial aldehyde dehydrogenase (mtALDH).
One of the challenges of the post-genomic era is how to assign functions to the many newly identified proteins that do not exhibit statistically significant sequence similarities to proteins with defined molecular functions. However, even when the predicted protein of a newly cloned gene exhibits statistically significant similarity to an ortholog with a defined function, there remain the tasks of first confirming the predicted function and then the more challenging problem of determining the precise metabolic role of that function within the organism. We consider this the “Post-Post-Genomic Challenge”.
The first of these tasks has been overcome for the rf2 gene. However, there still remains the significant challenge of determining the metabolic role of this enzyme. This task is complicated by the fact that ALDHs have many potential substrates, and is being addressed via a combination of biochemical, genetic and genomic approaches.