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Transcriptome and chromatin accessiblity analysis of mice soft palate to unreveal the role of Runx2 in regulating palate muscle development.

ABSTRACT: We report the application of single cell transcriptome, bulk transcriptome, and chromatin accessibility analysis for investigating the role of Runx2 in regulating soft palate muscle development. By isolating single cells from soft palate tissue of wild type embryos at E13.5, E14.5 and E15.5, we describe the heterogeneity of soft palate mesenchyme during development by analyzing single cell transcriptome. Combined analysis of bulk and single cell transcriptome of soft palate from wild type and Runx2 mutant suggests Runx2 activate expression of perimysial markers. Finally, we show that Runx2 activates expression of perimysial markers probably by repressing Twist1 through chromatin accessibility analysis. This study provides the first single cell level heterogeneity analysis of developing soft palate and shows the important role of Runx2 in regulating soft palate muscle development.

ORGANISM(S): Mus musculus

PROVIDER: GSE155928 | GEO | 2021/01/27

REPOSITORIES: GEO

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Project description:Nonsyndromic cleft palate is a common birth defect (1:700) with a complex etiology involving both genetic and environmental risk factors. Nicotine, a major teratogen present in tobacco products, was shown to cause alterations and delays in the developing fetus. To demonstrate the effect of nicotine on craniofacial development, particularly palatogenesis, we delivered three different doses of nicotine (1.5, 3.0 and 4.5 mg/kg/day) into pregnant BALB/c mice throughout their entire pregnancy using subcutaneous osmotic mini-pump. We assessed the pups for morphological anomalies, as well as genome-wide mRNA (transcriptome) microarray analysis. Consistent administration of nicotine caused developmental retardation, still birth, low birth weight, and significant palatal size and shape abnormality in the pups. However, it did not cause obvious cleft palate. The microarray data analysis using IPA identified differential expression of genes involved in various biological pathways, particularly cancer, genetic diseases, and tissue development in response to consistent nicotine exposure. 6232 up-regulated and 6310 down-regulated genes were detected in nicotine-treated groups compared to the control. Moreover, 45% of the genes associated with cleft palate were found to be affected by nicotine. Alterations of a subset of differentially expressed genes were illustrated with hierarchal clustering and RT-PCR. We concluded that consistent nicotine exposure during pregnancy interferes with normal growth and development of the fetus including palatogenesis; however, this interference does not result in cleft palate, rather smaller palate size with persistent MES. To our knowledge, this is the first experiment revealing the impact of nicotine on the fetal palate transcriptome in mice. Total 8 samples were analyzed. Using an osmotic minipump, duplicate samples from palates of either sterile physiological saline or nicotine (1.5 mg/kg/day, 3.0 mg/kg/day, or 4.5 mg/kg/day)-treated newborn pups.

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Transcriptome and chromatin accessiblity analysis of mice soft palate to unreveal the role of Runx2 in regulating palate muscle development.

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