A response regulator acquired via lateral gene transfer has rewired an ancestral genetic circuitry and regulates alternative pathogenic lifestyles.

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.

Molecular genetic analyses define the first homeostatic control pathway that maintains cell wall remodeling activity during bacterial growth.

Self-activating Aurora B kinase, opposed by an inhibitory phosphatase, forms spatial phosphorylation patterns during cell division.

Multicellular and socially aggregating prokaryotes contain previously undescribed, chaperone-based systems predicted to mediate defensive biological conflicts, several components of which are thematically similar antecedents of eukaryotic apoptosis pathways.

Minimal modifications of common regulatory circuits can allow bacteria to learn from the past to better predict the future, on a physiological, rather than evolutionary, timescale.

Post-implantation epiblast maturation and patterning of anterior-posterior axis in mouse embryonic development are mediated by pluripotency transcription factor Zfp281 through transcriptional and epigenetic control of Nodal signaling.

Structural analysis of the HipBST toxin–antitoxin system from E. coli shows how a toxin kinase has been split into two proteins and encodes its own inhibitor.

Realistic reaction-diffusion signaling networks that include cell-autonomous factors can robustly form self-organizing spatial patterns for any combination of diffusion coefficients without requiring differential diffusivity.

Cis-regulation such as enhancers and promoters plays a major role in parallel gene expression divergence and has features that make it a well-poised substrate for adaptive evolution.