Mycobacterium tuberculosis, which causes tuberculosis, can evolve rapidly in response to new environments by mutating genetic regulators that control multiple genes at once.

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.

Genetic architecture governs the evolvability of adaptive paths providing a framework for evolutionary forecasting.

A combination of genetics, experimental evolution and mathematical modelling defines information necessary to predict the outcome of short-term adaptive evolution.

Experimental evolution shows that when selection acts on two traits constrained by a trade-off, the direction of phenotypic evolution depends on the environment.

The ability to share resources for the benefit of all members of a group may have driven ancient organisms to evolve from a unicellular to a multicellular state.

Experimental evolution of yeast models of congenital disorders of glycosylation reveals that reduction, but not loss, of phosphoglucomutase activity best compensates for impaired phosphomannomutase activity.

A bacterial tRNA gene set rapidly evolves, compensating the loss of one tRNA type by large duplication events that increase the gene copy number of a second, different tRNA type.

Selective forces imposed by the squid animal host drive rapid adaptation of non-native Vibrio fischeri bacteria through convergent mutations of large effect, unmasking preexisting coordinated regulation of symbiosis.

A deep mutational coupling study demonstrates the ability of sequence coevolution methods to reveal the pattern of amino acid interactions underlying protein function.