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.

Interactions in protein complexes can be predicted from evolutionary information from genomic sequences.

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

The molecular mechanism of switching between phosphotransferase- and phosphatase-competent states in histidine-kinases has been uncovered, through direct crystallographic observation of bona fide complexes between a histidine-kinase and its response regulator from Bacillus subtilise.

Induction of the fission of mitochondria-populating sensory axons is shown to be a novel biological action of neurotrophins.

Activation by amino acids causes mTORC1 to translocate transiently to the lysosomal surface.

A protein within the nuclear membrane, MAN1, controls the expression of the circadian clock gene, BMAL1, in an example of cross-talk between two major gene regulatory pathways.

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

Complementary effects of FBF-1 and FBF-2 on germline stem cell dynamics result from their distinct cooperation with mRNA deadenylase resulting in the opposite effects on the shared target mRNAs.