Severe consequences of habitat fragmentation on genetic diversity of an endangered Australian freshwater fish: A call for assisted gene flow.

Genetic diversity underpins the ability of populations to persist and adapt to environmental changes. Substantial empirical data show that genetic diversity rapidly deteriorates in small and isolated populations due to genetic drift, leading to reduction in adaptive potential and fitness and increase in inbreeding. Assisted gene flow (e.g. via translocations) can reverse these trends, but lack of data on fitness loss and fear of impairing population "uniqueness" often prevents managers from acting. Here, we use population genetic and riverscape genetic analyses and simulations to explore the consequences of extensive habitat loss and fragmentation on population genetic diversity and future population trajectories of an endangered Australian freshwater fish, Macquarie perch Macquaria australasica. Using guidelines to assess the risk of outbreeding depression under admixture, we develop recommendations for population management, identify populations requiring genetic rescue and/or genetic restoration and potential donor sources. We found that most remaining populations of Macquarie perch have low genetic diversity, and effective population sizes below the threshold required to retain adaptive potential. Our simulations showed that under management inaction, smaller populations of Macquarie perch will face inbreeding depression within a few decades, but regular small-scale translocations will rapidly rescue populations from inbreeding depression and increase adaptive potential through genetic restoration. Despite the lack of data on fitness loss, based on our genetic data for Macquarie perch populations, simulations and empirical results from other systems, we recommend regular and frequent translocations among remnant populations within catchments. These translocations will emulate the effect of historical gene flow and improve population persistence through decrease in demographic and genetic stochasticity. Increasing population genetic connectivity within each catchment will help to maintain large effective population sizes and maximize species adaptive potential. The approach proposed here could be readily applicable to genetic management of other threatened species to improve their adaptive potential.

Integrative Approaches for Studying Mitochondrial and Nuclear Genome Co-evolution in Oxidative Phosphorylation.

In animals, interactions among gene products of mitochondrial and nuclear genomes (mitonuclear interactions) are of profound fitness, evolutionary, and ecological significance. Most fundamentally, the oxidative phosphorylation (OXPHOS) complexes responsible for cellular bioenergetics are formed by the direct interactions of 13 mitochondrial-encoded and ∼80 nuclear-encoded protein subunits in most animals. It is expected that organisms will develop genomic architecture that facilitates co-adaptation of these mitonuclear interactions and enhances biochemical efficiency of OXPHOS complexes. In this perspective, we present principles and approaches to understanding the co-evolution of these interactions, with a novel focus on how genomic architecture might facilitate it. We advocate that recent interdisciplinary advances assist in the consolidation of links between genotype and phenotype. For example, advances in genomics allow us to unravel signatures of selection in mitochondrial and nuclear OXPHOS genes at population-relevant scales, while newly published complete atomic-resolution structures of the OXPHOS machinery enable more robust predictions of how these genes interact epistatically and co-evolutionarily. We use three case studies to show how integrative approaches have improved the understanding of mitonuclear interactions in OXPHOS, namely those driving high-altitude adaptation in bar-headed geese, allopatric population divergence in Tigriopus californicus copepods, and the genome architecture of nuclear genes coding for mitochondrial functions in the eastern yellow robin.