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The transcription factor PROP1 controls a genetic network that drives pituitary stem cells to undergo an epithelial-to-mesenchymal-like transition and differentiate.

Airway cells are required for the maintenance of the adult mouse lung and for carcinogen-induced lung adenocarcinoma development, and are thus marked therapeutic targets.

In the pancreas, reciprocal interactions between epithelial cells and myeloid cells determine the balance between tissue repair and carcinogenesis by regulating acinar cell plasticity through differential activation of EGFR/MAPK signaling.

The planarian mex3-1 gene is required for non-stem cell fates and suppresses a stem cell fate in differentiating cells.

The transcriptional regulator YAP directs the specification and differentiation of stem cells that give rise to salivary gland ductal epithelium.

The Drosophila tracheal fate is stabilized by the combination of transcriptional programs to control tissue architecture and tissue-level input sensitive to tubular geometry, ensuring the robust mechanism of organ determination.

During ES cell differentiation, Yap1 directly regulates apoptosis-related genes like Bcl-2 and Mcl-1 to attenuate apoptosis and promote cell survival to allow for successful cell fate changes.

miR-34a prevents inflammation-induced colonic regeneration from oncogenesis by simultaneously targeting processes in both immune and epithelial cells, including T helper 17 cell differentiation, recruitment, and IL-17 induced epithelial proliferation.

An expandable cell population derived from human pluripotent stem cells exhibits properties of mesoderm and is restricted to differentiate into derivatives of intermediate mesoderm.

Improved characterisation of human embryonic lung development highlights human-mouse differences and facilitates the development of defined culture conditions for the expansion of self-renewing, multipotent human lung epithelial progenitor cells.