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.

In anticipation of a reward, hippocampal place cells simulate desired journeys through areas that have been seen, but not explored.

The acquisition of new foreign DNA by the prokaryotic adaptive immune system CRISPR-Cas is shown to depend on the fundamental sequence specificity of the Cas1 integrase.

The extra dimensions in protein sequence space open up indirect paths of adaptation and alleviate the constraint on the selective accessibility to high fitness genotypes.

The epistasis observed in TF-DNA binding preferences can be explained by the presence of two optima of very similar Gibbs energy that are located relatively far from each other in sequence space.

Cells must acquire multiple viral spacer sequences to neutralize mutant escaper phages and form colonies during the CRISPR-Cas immune response.

An experimentally supported model of grid cells naturally enables them to participate in firing sequences that encode rapid trajectories in space.

In a mouse model of neurodegeneration, hippocampal firing sequences that normally encode spatial memories become disengaged from external space.