Frank, S. A. and Barr, C. M. 2001. Spatial dynamics of cytoplasmic male sterility. Pages 219-243 in Integrating Ecology and Evolution in a Spatial Context. J. Silvertown and J. Antonovics, eds. Blackwell Science, Oxford.
Mitochondria sometimes cause male sterility in hermaphroditic plants by interfering with pollen development. Male-sterile plants usually produce more seeds than do hermaphrodites, probably because male sterility allows resources to be reallocated from pollen to seeds. Enhanced seed production benefits cytoplasmically inherited mitochondrial genes, which are transmitted through seeds but not through pollen. However, reduced pollen success lowers the fitness of nuclear genes, which are transmitted through both pollen and seeds. The different fitness consequences of male sterility for cytoplasmic and nuclear genes create a conflict of interest between these different subsets of the genome. Consistent with this idea of conflict, nuclear restorers occur that counteract cytoplasmic effects and restore pollen fertility.
Wild populations of cytoplasmically male-sterile plants typically have widespread polymorphisms of male-sterile mitochondria and nuclear restorer genes. These polymorphic genes appear to fluctuate over time and space, driven by the genomic conflict between the mitochondrial advantage of male sterility and the nuclear advantage of hermaphroditism. We review various theories that explain the dynamics of cytoplasmic male sterility. We also propose a new theory, the runaway allocation model, which predicts a positive association across species between the frequency of male-sterile plants and the seed productivity of male-sterile plants relative to hermaphrodites.
Finally, we review observations from wild populations of Plantago and Thymus. The data suggest that the movement of mitochondrial and nuclear genes in spatially subdivided metapopulations controls the spatiotemporal dynamics of male sterility. The data also show a positive association across species between the frequency of male sterility and the relative seed productivity of male steriles compared with hermaphrodites, supporting the main prediction of our runaway allocation model. Recent studies with molecular tools show great promise for tracking the movement of genes over space and unravelling the processes that drive cytoplasmic male sterility.