Pseudogenization of rcsD alters canonical Rcs phosphorelay signalling and marks a significant adaptive evolutionary step in the emergence of ubiquitous extant branches of Yersinia pestis that can maintain stable plague outbreaks.

In vivo and in vitro approaches uncover a new function for the β-barrel OmpA and reveal how it interacts with the stress sensor lipoprotein RcsF.

Mutations that block assembly of the interlocked RcsF/β barrel protein complex prevent detection of lipopolysaccharide stress and activation of Rcs signal transduction pathway.

Root causal genes correspond to the initial changes to gene expression that induce a diagnosis and can be reliably detected from bulk RNA-seq after determining a causal ordering from Perturb-seq.

A computational method reveals current sources along the dendritic tree of a single neuron of known morphology from extracellular potential.

Mice modelling atherosclerosis show neurovascular breakdown in the cortex compared to healthy controls, and inducing atherosclerosis in mice modelling Alzheimer's disease increases the number of amyloid plaques in the hippocampus.

Stimulus-induced causal interactions in the gamma range can flow in direction opposite to the canonical microcircuit, violating the notion that they are signatures of feedforward communication.

Cryo-EM structures uncover glycosylation in the ectodomains of full-length HER4 homodimer and HER2/HER4 heterodimer complexes, revealing how the binding of various growth factors alters dynamics at the dimerization interface.

Cryo-electron microscopic structures of 5-HT₃A receptor in complex with first and second generations of clinically used setron reveal the molecular basis for their binding modes and mechanisms of inhibitory action.

The probability of a cellular response to a differentiation inducing signal is correlated with the dynamic expression of a Ras protein, and produces a ‘salt and pepper’ pattern of cell differentiation.