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Malaria parasites avoid destruction by their host's immune response through systematic and coordinated expression switching between members of a network of variant antigen-encoding genes, a process that is mediated by a uniquely conserved gene called var2csa.

The nearly universal nature of scaled cell shape variability in an epithelial monolayer is unavoidable, irrespective of health or disease, as it comes from a mathematical property.

Infants' vocalisations are contingent on their own stress physiology, and alter the inter-personal dynamics of how stress states are shared across the infant-caregiver dyad.

A novel experimental approach reveals how mechanical force acting on the skin is converted into electrical signaling in sensory neurons to evoke the sensation of touch.

Age-stratified comparisons of gene expression in progeria patient fibroblasts reveals disruption of mesenchymal lineage pathways and points to a deficit in chondrogenic commitment in early development and a depletion of the mesenchymal lineage stem cell pool.

In bacteria, frequent adaptive copy-number mutations can hinder the fixation of beneficial point mutations and hence the divergence of duplicated DNA sequences.

The maintenance of skeletal muscle function improves the quality of life, and therefore understanding how changes in the genome drive changes in the skeletal muscle proteome has revealed novel regulators of muscle physiology.

The modelled structure of a membrane protein supports the hypothesis that it has a new fold with a channel that allows a chemical group to cross the membrane to decorate surface structures.

Invariant natural killer T (iNKT) cells have some shared yet some distinct metabolic and transcriptional programs for their in vivo effector functions, including a novel population of memory-like regulatory iNKT cells.

Dominant mutations in Arl3, linked to inherited retinal dystrophy, disrupt the active Arl3-GTP ciliary gradient and cause a defect in rod photoreceptor nuclear migration that can be rescued by elevating ciliary Arl3 activity or reducing aberrant non-ciliary Arl3 activity.