Perturbations in the extracellular environment drive transitions from a highly stable memory state to an alternative phenotype in microorganisms.

Accumulation of succinate during the in vitro modeling of embryonic stem cell state transition critically regulate cell fate.

Time-course phosphoproteomics reveals that selective dephosphorylation is critical for directing the MI/MII transition and that, through its inherent phospho-threonine preference, PP2A-B55 imposes specific phosphoregulated behaviors that distinguish the two meiotic divisions.

The conformational switch of ABCG2 from the high substrate affinity inward-facing to a low substrate affinity outward-facing state is induced by nucleotide binding and accelerated by transported substrates.

Quantitative single molecule and super resolution imaging in mammalian cells reveal a population of precursor aggregates describable by first order phase transition theory.

The gating polarity of a voltage-gated ion channel is primarily determined by turn propensity of residues at a critical position in the middle of the S4 voltage-sensing helix.

A computational model shows that natural selection can cause populations to evolve a distinctive population-level phenotype: the ability to transition between collective states in response to the environment.

Compressive force spectroscopy of single molecules reveals that intra-protein forces underlie the long-distance coordination of structural changes within a cytotoxin during pore formation.

Soon after fertilisation, a critical portion of the embryonic genome is switched on through the actions of maternally inherited Stella, in part through controlling the activation of transposable elements.

Behavioral pharmacology and molecular biology reveal a translational control mechanism underlying auditory imprinting and structural plasticity that can be pharmacologically manipulated to reopen the critical period.