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Thymus ageing is characterised by both compositional and transcriptional shifts amongst epithelial cells that perturb their differentiation, contribute to organ atrophy and ultimately impair immune function.

Chronic fat overload triggers the conversion of quiescent biliary epithelial cells into proliferative progenitors through an E2F-dependent mechanism.

Time-lapse imaging and the modular recreation of host physiology reveal that alveolar epithelial cells, potential permissive infection sites for Mycobacterium tuberculosis, can restrict early bacterial growth via surfactant secretion.

Breast luminal epithelial cells are the hotspots of aging-associated changes, which prime aged epithelia for oncogenic gene activation and may explain individual differences in breast cancer susceptibility due to the aging-associated increase in gene expression variances in luminal epithelia.

Studies of organoid morphogenesis, combined with proteomics and molecular profiling, identify the THBS1-YAP axis as a signalling mechanism that mediates paracrine communication between tumour cells and their wildtype epithelial neighbours.

In response to disruption of barrier functions mediated by septate junctions, Drosophila epithelial cells restrict endosomal degradation of transmembrane cell adhesion proteins to promote their recycling in order to maintain tissue integrity.

Stress fibers with multiple adhesions along their lengths and treadmilling dynamics may help migrating epithelial cells maintain a linear trajectory and thereby reinforce their collective motility.

Knocking out Folliculin (FLCN) in human renal epithelial cells activates STAT1/2-mediated gene expression, independent of interferon, uncovering a tissue-specific process potentially relevant in the cancer syndrome Birt-Hogg-Dubé (BHD).

Lung stem cell niche aging is associated with altered bioenergetics, metabolic dysfunction, and senescence of mesenchymal stromal cells that restricts 3D organoid, or alveolosphere formation, potentially accounting for reduced regenerative capacity with aging.

Parallel studies in primary human airway cells and stem cell-derived enteroids show that Enterovirus D-68 differentially infects and induces innate immune signaling in the respiratory and intestinal epithelium.