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Development. 2019 Feb 11;146(3). pii: dev171496. doi: 10.1242/dev.171496.

Wnt/Fgf crosstalk is required for the specification of basal cells in the mouse trachea.

Author information

1
Center for Human Development, Department of Medicine, Columbia University Medical Center, NY 10032, USA.
2
Tianjin Haihe Hospital, Tianjin 300350, P.R. China.
3
Haihe Clinical College of Tianjin Medical University, Tianjin 301700, P.R. China.
4
Center for Human Development, Department of Medicine, Columbia University Medical Center, NY 10032, USA jq2240@cumc.columbia.edu mj2735@cumc.columbia.edu.

Abstract

Basal progenitor cells are crucial for the establishment and maintenance of the tracheal epithelium. However, it remains unclear how these progenitor cells are specified during foregut development. Here, we found that ablation of the Wnt chaperone protein Gpr177 (also known as Wntless) in mouse tracheal epithelium causes a significant reduction in the number of basal progenitor cells accompanied by cartilage loss in Shh-Cre;Gpr177loxp/loxp mutants. Consistent with the association between cartilage and basal cell development, Nkx2.1+p63+ basal cells are co-present with cartilage nodules in Shh-Cre;Ctnnb1DM/loxp mutants, which maintain partial cell-cell adhesion but not the transcription regulation function of β-catenin. More importantly, deletion of Ctnnb1 in the mesenchyme leads to the loss of basal cells and cartilage, concomitant with reduced transcript levels of Fgf10 in Dermo1-Cre;Ctnnb1loxp/loxp mutants. Furthermore, deletion of Fgf receptor 2 (Fgfr2) in the epithelium also leads to significantly reduced numbers of basal cells, supporting the importance of Wnt/Fgf crosstalk in early tracheal development.

KEYWORDS:

Airway; Basal progenitor; Cartilage; Fgf; Mouse; Wnt/β-catenin; Wntless

PMID:
30696710
PMCID:
PMC6382003
[Available on 2020-02-01]
DOI:
10.1242/dev.171496

Conflict of interest statement

Competing interestsThe authors declare no competing or financial interests.

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