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Published on: May 5, 2016
Disruption of Cdyl gene impairs mouse lung epithelium differentiation and maturation
Li Wan1, Xiaojun Hu2, Tian Xia3
1Clinical Laboratory, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou 510260, China; Center for Stem Cell Biology and Tissue Engineering, Key Laboratory for Stem Cells and Tissue Engineering, Ministry of Education, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Abstract:
CDYL is a chromodomain protein that has been identified as a transcriptional co-repressor that is primarily involved in the formation of repressor complexes which coordinate histone modifications to repress gene transcription. However, most functions and mechanisms of action of the CDYL protein are unknown. In this study, we show that Cdyl-/- mice died of respiratory distress immediately at birth because of distinct abnormalities in distal lung morphogenesis which was characterized by thickened septal and expiratory alveolus atelectasis. Furthermore, Cdyl deletion in mice led to excessive proliferation of immature epithelial cells and an arrest in alveolar epithelium cell differentiation in late gestation which were associated with decreased secretion of mature surfactant proteins in alveolus. Microarray analysis showed that Cdyl gene deletion influenced the expression of genes regulating neuroactive ligand-receptor interactions, cell adhesion, and cell cycle. We validated that Cdyl repressed the transcriptional activity of Cks1 in vitro. In conclusion, Cdyl gene participates in the perinatal respiratory epithelium differentiation and maturation that is important for normal lung function at birth.
Insights
The CDYL gene is crucial for lung development. Its absence in mice caused severe respiratory problems and abnormal lung structure at birth, indicating its importance in perinatal lung maturation.
Area of Science:
- Molecular Biology
- Developmental Biology
- Genetics
Background:
- CDYL (chromodomain Y like) is a transcriptional co-repressor involved in gene silencing through histone modification.
- The precise functions and mechanisms of CDYL in mammalian development remain largely uncharacterized.
Purpose of the Study:
- To investigate the role of the CDYL gene in lung development and perinatal respiratory function.
- To elucidate the molecular mechanisms underlying CDYL's function in lung morphogenesis.
Main Methods:
- Analysis of Cdyl knockout (Cdyl-/-) mice.
- Histological examination of lung tissue to assess morphology and cell differentiation.
- Microarray analysis to identify gene expression changes upon Cdyl deletion.
- In vitro validation of CDYL's transcriptional repression activity on target genes.
Main Results:
- Cdyl-/- mice exhibited immediate respiratory distress and mortality at birth due to severe lung developmental abnormalities.
- Defects included thickened septa, alveolar atelectasis, excessive proliferation of immature epithelial cells, and impaired alveolar cell differentiation.
- Cdyl deletion altered gene expression related to neuroactive ligand-receptor interactions, cell adhesion, and cell cycle, and repressed Cks1 transcription in vitro.
Conclusions:
- The CDYL gene plays a critical role in perinatal respiratory epithelium differentiation and maturation.
- Proper lung function at birth is dependent on the normal function of CDYL during late gestation and perinatal development.
