Epithelial inactivation of Yy1 abrogates lung branching morphogenesis

Development
Olivier BoucheratLucie Jeannotte

Abstract

Yin Yang 1 (YY1) is a multifunctional zinc-finger-containing transcription factor that plays crucial roles in numerous biological processes by selectively activating or repressing transcription, depending upon promoter contextual differences and specific protein interactions. In mice, Yy1 null mutants die early in gestation whereas Yy1 hypomorphs die at birth from lung defects. We studied how the epithelial-specific inactivation of Yy1 impacts on lung development. The Yy1 mutation in lung epithelium resulted in neonatal death due to respiratory failure. It impaired tracheal cartilage formation, altered cell differentiation, abrogated lung branching and caused airway dilation similar to that seen in human congenital cystic lung diseases. The cystic lung phenotype in Yy1 mutants can be partly explained by the reduced expression of Shh, a transcriptional target of YY1, in lung endoderm, and the subsequent derepression of mesenchymal Fgf10 expression. Accordingly, SHH supplementation partially rescued the lung phenotype in vitro. Analysis of human lung tissues revealed decreased YY1 expression in children with pleuropulmonary blastoma (PPB), a rare pediatric lung tumor arising during fetal development and associated with DICER1 mut...Continue Reading

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Citations

Oct 20, 2017·European Journal of Pediatrics·Claire LeblancSabine Irtan
Feb 19, 2020·PLoS Computational Biology·Chieh LinZiv Bar-Joseph
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May 24, 2021·Developmental Biology·Nicole A EdwardsAaron M Zorn
Jun 17, 2021·American Journal of Physiology. Lung Cellular and Molecular Physiology·Kevin Y Huang, Enrico Petretto

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