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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.

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.

Rationally designed peptide inhibitors of human voltage-gated channels have transformative potential to define a new class of biologics to treat pain.

HOTAIR is required in an ongoing manner when it regulates epigenetic status and reprograms cancer cell gene expression in promoting breast cancer metastasis.