What are the genomic foundations of adaptation in sexual populations? We address this question using fitness–character and whole-genome sequence data from 30 Drosophila laboratory populations. These 30 populations are part of a nearly 40-year laboratory radiation featuring 3 selection regimes, each shared by 10 populations for up to 837 generations, with moderately large effective population sizes. Each of 3 sets of the 10 populations that shared a selection regime consists of 5 populations that have long been maintained under that selection regime, paired with 5 populations that had only recently been subjected to that selection regime. We find a high degree of evolutionary parallelism in fitness phenotypes when most-recent selection regimes are shared, as in previous studies from our laboratory. We also find genomic parallelism with respect to the frequencies of single-nucleotide polymorphisms, transposable elements, insertions, and structural variants, which was expected. Entirely unexpected was a high degree of parallelism for linkage disequilibrium. The evolutionary genetic changes among these sexual populations are rapid and genomically extensive. This pattern may be due to segregating functional genetic variation that is abundantly maintained genome-wide by selection, variation that responds immediately to changes of selection regime.

The well-supported molecular phylogeny provides evidence for delineation of subfamilies within core Asparagales. With advances in technology and bioinformatics tools, the use of massively parallel sequencing will continue to become easier and more affordable for phylogenomic and molecular evolutionary biology investigations.

Resolution of evolutionary relationships among some monocot orders remains problematic despite the application of various taxon and molecular locus sampling strategies. In this study we sequenced and analysed a fragment of the low‐copy, nuclear phytochrome C (PHYC) gene and combined these data with a previous multigene data set (four plastid, one mitochondrial, two nuclear ribosomal loci) to determine if adding this marker improved resolution and support of relationships among major lineages of monocots. Our results indicate the addition of PHYC to the multigene dataset increases support along the backbone of the monocot tree, although relationships among orders of commelinids remain elusive. We also estimated divergence times in monocots by applying newly evaluated fossil calibrations to our resolved phylogenetic tree. Inclusion of early‐diverging angiosperm lineages confirmed the origin of extant monocots c. 131 Mya and strengthened the hypothesis of recent divergence times for some lineages, although current divergence time estimation methods may inadequately model rate heterogeneity in monocots. We note significant shifts in diversification in at least two monocot orders, Poales and Asparagales. We describe patterns of diversification in the context of radiation of other relevant plant and animal lineages. © 2015 The Linnean Society of London, Botanical Journal of the Linnean Society, 2015, 178, 375–393.

Mitochondria from normal and cancerous cells represent a tale of two cities, wherein both execute similar processes but with different cellular and molecular effects. Given the number of reviews currently available which describe the functional implications of mitochondrial mutations in cancer, this article focuses on documenting current knowledge in the abundance and distribution of somatic mitochondrial mutations, followed by elucidation of processes which affect the fate of mutations in cancer cells. The conclusion includes an overview of translational implications for mtDNA mutations, as well as recommendations for future research uniting mitochondrial variants and tumorigenesis.