Mitochondrial function is achieved through the cooperative interaction of two genomes: one nuclear (nuDNA) and the other mitochondrial (mtDNA). The unusual transmission of mtDNA, predominantly maternal without recombination is predicted to affect the fitness of male offspring. Recent research suggests the strong sexual dimorphism in aging is one such fitness consequence. The uniparental inheritance of mtDNA results in a selection asymmetry; mutations that affect only males will not respond to natural selection, imposing a male‐specific mitochondrial mutation load. Prior work has (...) implicated this male‐specific mutation load in disease and infertility, but new data from fruit flies suggests a prominent role for mtDNA in aging; across many taxa males almost invariably live shorter lives than females. Here we discuss this new work and identify some areas of future research that might now be encouraged to explore what may be the underpinning cause of the strong sexual dimorphism in aging.Editor's suggested further reading in BioEssays: Mitonuclear match: Optimizing fitness and fertility over generations drives ageing within generations AbstractMitochondrial manoeuvres: Latest insights and hypotheses on mitochondrial partitioning during mitosis in Saccharomyces cerevisiae AbstractMitochondria and the culture of the Borg Abstract. (shrink)

Mitochondria, the powerhouses of our cells, are essential to life. Normal mitochondrial function is achieved through the cooperative interaction of the nuclear and mitochondrial genomes. New IVF approaches intended to circumvent devastating mitochondrial disease look set to change the ancient pattern of mtDNA inheritance and interaction with unknown consequences.

The human Y chromosome contains very low levels of nucleotide variation. It has been variously hypothesized that this invariance reflects historic reductions in the human male population, a very recent common ancestry, a slow rate of molecular evolution, an inability to evolve adaptively, or frequent selective sweeps acting on genes borne on the Y chromosome. We propose an alternative theory in which human Y chromosome evolution is driven by mutations in the maternally inherited mitochondrial genome, which impair male fertility and (...) ultimately lead to a reduction in the effective population size (Ne) and consequently the variability of the Y chromosome. BioEssays 24:275–279, 2002. © 2002 Wiley Periodicals, Inc.; DOI 10.1002/bies.10062. (shrink)

Microsatellites are among the most versatile of genetic markers, being used in an impressive number of biological applications. However, the evolutionary dynamics of these markers remain a source of contention. Almost 20 years after the discovery of these ubiquitous simple sequences, new genomic data are clarifying our understanding of the structure, distribution and variability of microsatellites in genomes, especially for the eukaryotes. While these new data provide a great deal of descriptive information about the nature and abundance of microsatellite sequences (...) within eukaryotic genomes, there have been few attempts to synthesise this information to develop a global concept of evolution. This review provides an up‐to‐date account of the mutational processes, biases and constraints believed to be involved in the evolution of microsatellites, particularly with respect to the creation and degeneration of microsatellites, which we assert may be broadly viewed as a life cycle. In addition, we identify areas of contention that require further research and propose some possible directions for future investigation. BioEssays 28: 1040–1050, 2006. © 2006 Wiley Periodicals, Inc. (shrink)