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.
Predictable patterns of fitness evolution observed in microbial evolution experiments can emerge generically as a consequence of widespread epistatic interactions between mutations.
Drug resistance in HIV is the result of mutations, which affect fitness depending on epistatic interactions with the entire sequence background that varies within and between patient populations.
Pairwise combinations of growth-promoting genes regulating distinct cellular mechanisms lead to synergistic effects on leaf growth, and hence greatly increased leaf size.
Mutations that affect a metabolic network generically exhibit epistasis, which propagates to higher level phenotypes, such as fitness, carrying some information about the network’s topology.
Greater phenotypic variation is exposed by mutations in a gene regulatory system compared to mutations in its constitutive components, namely the transcription factor and the promoter, alone.
Some of the mutations that occur during influenza evolution can only be tolerated in conjunction with other mutations that increase the stability of a viral protein.
Multiple replicated examples of epistasis affecting gene expression in humans are identified, some explaining a substantial proportion of the variation in expression.
Short peptides that bind tightly to anti-apoptotic protein Bfl-1 but not other Bcl-2 family members provide a tool for diagnosing cancer cell survival mechanisms and a lead for developing new therapeutics.
