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Stress ball morphogenesis: how the lizard builds its lung

ABSTRACT: Stress ball morphogenesis: how the lizard builds its lung

PROVIDER: PRJNA719416 | ENA |

REPOSITORIES: ENA

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Stress ball morphogenesis: how the lizard builds its lung

Project description:Lung function is closely coupled to its structural anatomy, which varies greatly across vertebrates. Although architecturally simple, a complex pattern of airflow is thought to be achieved in the lizard lung due to its cavernous central lumen and honeycomb-shaped wall. We find that the wall of the lizard lung is generated from an initially smooth epithelial sheet, which is pushed through holes in a hexagonal smooth muscle meshwork by forces from fluid pressure, similar to a stress ball. By combining next-generation sequencing with timelapse imaging, we reveal that the hexagonal smooth muscle geometry self-assembles in response to circumferential and axial stresses downstream of pressure. A quantitative computational model predicts the pressure-driven changes in epithelial topology, which we replicate using a 3D-printed engineered tissue model of optogenetically-driven smooth muscle contraction. These results reveal the physical principles used to sculpt the unusual architecture of the lizard lung, which could be exploited as a novel strategy to engineer tissues.

2021-04-03 | GSE171416 | GEO

Stress ball morphogenesis: How the lizard builds its lung.

Project description: Not available

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Gene expression profile at single-cell level of regenerating lizard (Anolis carolinensis) tail

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Epithelial inactivation of Yy1 abrogates lung branching morphogenesis

Project description: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 while 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 those seen in human congenital cystic lung diseases. The cystic lung phenotype in Yy1 mutants can be explained by the reduced expression of Shh in lung endoderm, a transcriptional target of YY1, 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 mutations. No evidence for a potential genetic interplay between murine Dicer and Yy1 genes during lung morphogenesis was observed. However, the cystic lung phenotype resulting from the epithelial inactivation of Dicer function mimics the Yy1 lung malformations with similar changes in Shh and Fgf10 expression. Together, our data demonstrate the critical requirement for YY1 in lung morphogenesis and identify Yy1 mutant mice as a potential model for studying the genetic basis of PPB.

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Transcription profiling of mouse TGF-a induction in saccular phase and alveolar phase lung morphogenesis in mice

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Fibroblast growth factor (FGF) 10 is essential for lung morphogenesis

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