skip to primary navigationskip to content

25.06.15 Rawlins and Simons groups at the Gurdon Institute find two distinct populations of basal cells in airway epithelium

last modified Jul 15, 2015 06:26 PM
New findings from the Rawlins and Simons labs on cell lineage in slow-turnover airway epithelium, published in Cell Reports, 7th July 2015 issue
25.06.15 Rawlins and Simons groups at the Gurdon Institute find two distinct populations of basal cells in airway epithelium

Graphical abstract from the paper

Clonal Dynamics Reveal Two Distinct Populations of Basal Cells in Slow Turnover Airway Epithelium

Watson et al., 2015, Cell Reports 12, pp 90-101

July 7, 2015


The Rawlins and Simons groups have collaborated to investigate the steady-state, slow turnover of cells lining the mouse trachea to find out how the different mature cell types are generated from the adult stem cells. It is already known that human cells have a very similar cell lineage to mouse trachea, but the details of the hierarchy are easier to explore in the mouse. The cell population includes basal cells and luminal secretory cells and ciliated cells. 

Using clonal lineage labelling, mathematical modelling, and single-cell molecular analysis, the team have shown that the mouse tracheal epithelium contains two major, equally distributed subpopulations of basal cells: stem cells and long-lived precursors that are already committed to differentiation. These two cell types are morphologically identical.  The precursors mature after 11 days into luminal secretory cells, which are short-lived and self renewing, and which are the major steady-state source of new ciliated cells.

Having two populations of basal cells, one committed to differentiation yet morphologically identical to the stem cells, is an unexpected mechanism of epithelial maintenance in a slow-turnover tissue.  The model presents a new experimental and theoretical foundation for studies of airway homeostasis, injury and disease.


More about the Rawlins group and the Simons group

Image reproduced from the paper under Creative Commons CC-BY license.

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