The DNA-bridging efficiency of H-NS, a genome organising and transcription regulatory protein, is modulated by changes in environmental conditions of the cell, which drive a structural rearrangement of the protein.

Combining in silico and experimental approaches to identify and understand the residue changes in the H-NS protein that allowed bacteria to adapt environment-sensing to different habitats.

Bridged H-NS filaments inhibit transcript elongation by bacterial RNA polymerase by enhancing backtracking and increasing Rho-dependent termination at a subset of pause sites that are normally poor Rho substrates.

Quantification of both viral transcription and progeny production from single influenza-infected cells shows that the cells that produce the most viral RNA often do not produce the most virions.

Re-characterization of the targets of a commonly used nuclear speckle marker unexpectedly leads to the discovery of the elusive core of the nuclear speckles.

Mutating a highly conserved intramembrane salt bridge unmasks structural and functional coupling between channel gating and ion permeation in the muscle nicotinic receptor.

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

Genetic and molecular analysis of TP53 exon-6 truncating mutations reveal that these mutations, contrary to current belief, promote tumorigenesis and point towards strategies for treating cancers driven by these prevalent mutations.

The transcriptomes of hematopoietic stem and progenitor cells of human juvenile myelomonocytic leukemia patients and a zebrafish model for Noonan syndrome reveal a common inflammatory response, which may have a causal role in associated myeloproliferative neoplasm.

Efficiency measures the fundamental link between agonist binding and protein conformational change, and in nicotinic receptors has 5 values that calibrate energy changes in the induced fit that triggers activation.