Correction: Transcriptome profiling of mouse brain and lung under Dip2a regulation using RNA-sequencing

Sah, Rajiv Kumar; Yang, Anlan; Bah, Fatoumata Binta; Adlat, Salah; Bohio, Ameer Ali; Oo, Zin Mar; Wang, Chenhao; Myint, May Zun Zaw; Bahadar, Noor; Zhang, Luqing; Feng, Xuechao; Zheng, Yaowu

doi:10.1371/journal.pone.0225570

Cited by 1 publication

(3 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Two hours later, mice were sacrificed and embryos were harvested. Lungs from all embryos were removed and embedded in OCT, sectioned in cryostat microtome, and processed for immunohistochemical evaluation [24]. BrdU was revealed using the Anti-BrdU antibody (Rat monoclonal, Abcam Cat#ab6326) for 1.5 h at room temperature.…”

Section: -Bromo-2-deoxy-uridine (Brdu) Labelingmentioning

confidence: 99%

“…4.11. RNA-Sequencing (RNA-Seq) RNA-seq of E18.5 lungs was carried out as described before (Sah et al, 2019) using Illumina HiseqTM 2500 (Biomarker, Beijing, China). A total of three pairs of RNA samples (3 WT and 3 Dip2b tm1a/tm1a ) were sequenced.…”

Section: Tunel Assaymentioning

confidence: 99%

“…Dip2A have a functional role in acetyl-coenzyme A (acetyl-CoA) synthesis [23]. We have also studied the transcriptome of E18.5 embryonic lung and brain under Dip2a regulation [24].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Targeted Disruption of Mouse Dip2B Leads to Abnormal Lung Development and Prenatal Lethality

Sah

Bah

et al. 2020

IJMS

Self Cite

View full text Add to dashboard Cite

Molecular and anatomical functions of mammalian Dip2 family members (Dip2A, Dip2B and Dip2C) during organogenesis are largely unknown. Here, we explored the indispensable role of Dip2B in mouse lung development. Using a LacZ reporter, we explored Dip2B expression during embryogenesis. This study shows that Dip2B expression is widely distributed in various neuronal, myocardial, endothelial, and epithelial cell types during embryogenesis. Target disruption of Dip2b leads to intrauterine growth restriction, defective lung formation and perinatal mortality. Dip2B is crucial for late lung maturation rather than early-branching morphogenesis. The morphological analysis shows that Dip2b loss leads to disrupted air sac formation, interstitium septation and increased cellularity. In BrdU incorporation assay, it is shown that Dip2b loss results in increased cell proliferation at the saccular stage of lung development. RNA-seq analysis reveals that 1431 genes are affected in Dip2b deficient lungs at E18.5 gestation age. Gene ontology analysis indicates cell cycle-related genes are upregulated and immune system related genes are downregulated. KEGG analysis identifies oxidative phosphorylation as the most overrepresented pathways along with the G2/M phase transition pathway. Loss of Dip2b de-represses the expression of alveolar type I and type II molecular markers. Altogether, the study demonstrates an important role of Dip2B in lung maturation and survival.

show abstract

Section: -Bromo-2-deoxy-uridine (Brdu) Labelingmentioning

confidence: 99%

Section: Tunel Assaymentioning

confidence: 99%