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Prmt5 promotes ciliated cell specification of airway epithelial progenitors via transcriptional inhibition of Tp63.


ABSTRACT: The epithelium of the pulmonary airway is composed of several distinct cell types that differentiate from common progenitor cells to provide defense against environmental insults. Epigenetic mechanisms regulating lineage differentiation of airway epithelial progenitors remain poorly understood. Protein arginine methyltransferase 5 (Prmt5) is a predominant type II arginine methyltransferase that methylates >85% of symmetric arginine residues. Here, we provide evidence for the function of Prmt5 in promoting ciliated cell fate specification of airway epithelial progenitors. We show that lung epithelial-specific deletion of Prmt5 resulted in a complete loss of ciliated cells, an increased number of basal cells, and ecotopic-expressed Tp63-Krt5+ putative cells in the proxi

SUBMITTER: Li Q 

PROVIDER: S-EPMC10392137 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature