skip to primary navigationskip to content

18.10.16 Emma Rawlins' group shows that extrinsic signals drive lung epithelial cell fate

last modified Oct 25, 2016 10:31 AM
In this Development paper, the Rawlins group with colleagues in Edinburgh investigate the mechanisms controlling the fate of developing lung epithelial cells
18.10.16 Emma Rawlins' group shows that extrinsic signals drive lung epithelial cell fate

Excerpt from Fig. 2: Sections of mouse lungs with labelled progenitor grafts.

Lung epithelial tip progenitors integrate glucocorticoid- and STAT3-mediated signals to control progeny fate

Usua Laresgoiti, Marko Z. Nikolić, Chandrika Rao, Jane L. Brady, Rachel V. Richardson, Emma J. Batchen, Karen E. Chapman & Emma L. Rawlins, Development (2016) 143: 3686-3699; doi: 10.1242/dev.134023


The epithelial cells found at the distal tips of the developing lung comprise a multipotent progenitor population. During development, these cells first give rise to bronchiolar cells, which form the conducting airways, but then switch to producing alveolar cells, which form the sites of gas exchange.

In this paper, Emma Rawlins and co-workers investigate the factors that control this transition in the mouse lung. They report that distal tip progenitors begin to express alveolar fate markers at around E16.5. Using a grafting assay, the researchers reveal that extrinsic, rather than intrinsic, factors determine the fate of tip progenitors. Importantly, they reveal that the glucocorticoid and STAT3 signalling pathways operate in parallel to promote alveolar fate; both pathways are sufficient but not necessary for specifying alveolar cells. Finally, the authors demonstrate that STAT3 signalling is also active at a similar stage of lung development in humans.

Overall, these results highlight that the fate of lung epithelial cells is controlled by extrinsic signalling from surrounding tissues, a finding that has important implications for developing therapies that can restore alveolar capacity in human lungs.



Text above derived from feature article in Development, under Creative Commons (CC BY 4.0).


Read more about research in the Rawlins lab.

Watch Emma Rawlins describe her research on video.

Studying development to understand disease

The Gurdon Institute is funded by Wellcome and Cancer Research UK to study the biology of development, and how normal growth and maintenance go wrong in cancer and other diseases.

combinedLogo x3 trans2018


Share this

A walk through tau therapeutic strategies

Labeling strategies matter for super-resolution microscopy: a comparison between HaloTags and SNAP-tags

Stem Cell-Derived Human Gametes: The Public Engagement Imperative

Tissue- and sex-specific small RNAomes reveal sex differences in response to the environment

Comparative Epigenomics Reveals that RNA Polymerase II Pausing and Chromatin Domain Organization Control Nematode piRNA Biogenesis

Pluripotency and X chromosome dynamics revealed in pig pre-gastrulating embryos by single cell analysis

Constrained actin dynamics emerges from variable compositions of actin regulatory protein complexes

Microtubules Deform the Nuclear Membrane and Disrupt Nucleocytoplasmic Transport in Tau-Mediated Frontotemporal Dementia

Drosophila IMP regulates Kuzbanian to control the timing of Notch signalling in the follicle cells

Challenges in unsupervised clustering of single-cell RNA-seq data

Engineering vasculature: Architectural effects on microcapillary-like structure self-assembly

ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

Altered γ-Secretase Processing of APP Disrupts Lysosome and Autophagosome Function in Monogenic Alzheimer’s Disease

Helicase subunit Cdc45 targets the checkpoint kinase Rad53 to both replication initiation and elongation complexes after fork stalling

Competition for Mitogens Regulates Spermatogenic Stem Cell Homeostasis in an Open Niche

Link to full list on PubMed