Replicating experimental evolution from ancestral proteins shows that historical contingency steadily overwhelms chance and necessity as the primary cause of evolutionary variation in molecular sequences on long phylogenetic timescales.

The evolution of the light-sensitive visual pigment rhodopsin involved functional tradeoffs that may have sacrificed rod photosensitivity for active-state protein stability to mitigate phototoxicity in tetrapods, but not in fishes.

A long-term evolution experiment with Escherichia coli shows that the appearance and optimization of a new trait can require both co-opting existing cellular pathways for new roles and reversing a history of previous adaptation.

Experimentally reconstructing the evolution of the molecular complex that animals use to orient the mitotic spindle establishes a simple genetic and physical mechanism for the emergence of a function essential for multicellularity.

Combined antigenic and genetic analysis shows that different strains of the human influenza virus display dramatically different rates of antigenic drift, and that these differences have a significant impact on the number of new infections in each flu season.

Transgenic animals carrying reconstructed ancestral alleles reveal how two ancient mutations allowed a regulatory protein to evolve a controlling role in embryonic development in flies.

The HMA domains of Pikp-1 and Pikm-1 NLR receptors have convergently evolved to bind AVR-PikD with high affinity through distinct evolutionary and biochemical paths.

Phylogenetic relationships between viral RNA segments are distinct between subtypes and lineages of seasonal human influenza A viruses and implicate RNA-RNA relationships as novel drivers of influenza virus evolution.

Experimental mapping of the joint sequence space of an ancient transcription factor (TF) and its DNA binding sites reveals that epistasis across the molecular interface permitted the evolution of a new and specific TF-DNA complex.

Human cell lines regress to become ‘de-sexualized’ by reconfiguring to a 2:3 X/A ratio of high fitness, thus shedding light on the evolution of mammalian sex chromosomes.