PubMed:31241704 JSONTXT

{"project":"PubMed_ArguminSci","denotations":[{"id":"T1","span":{"begin":125,"end":226},"obj":"DRI_Background"},{"id":"T2","span":{"begin":227,"end":408},"obj":"DRI_Approach"},{"id":"T3","span":{"begin":409,"end":579},"obj":"DRI_Background"},{"id":"T4","span":{"begin":580,"end":823},"obj":"DRI_Background"},{"id":"T5","span":{"begin":824,"end":964},"obj":"DRI_Background"},{"id":"T6","span":{"begin":984,"end":1104},"obj":"DRI_Background"},{"id":"T7","span":{"begin":1183,"end":1302},"obj":"DRI_Outcome"},{"id":"T8","span":{"begin":1303,"end":1538},"obj":"DRI_Background"}],"text":"Position-dependent correlation between TBX22 exon 5 methylation and palatal shelf fusion in the development of cleft palate.\nDNA methylation is essential for spatiotemporally-regulated gene expression in embryonic development. TBX22 (Chr X: 107667964-107688978) functioning as a transcriptional repressor affects DNA binding, sumoylation, and transcriptional repression associated with X-linked cleft palate. This study aimed to explore the relationship and potential mechanism between TBX22 exon 5 methylation and palatal shelf fusion induced by all-trans retinoic acid (ATRA). We performed DNA methylation profiling, using MethylRAD-seq, after high throughput sequencing of mouse embryos from control (n=9) and ATRA-treated (to induce cleft palate, n=9) C57BL/6J mice at embryonic gestation days(E) 13.5, 14.5 and 16.5. TBX22 exon 5 was hyper-methylated at the CpG site at E13.5 (P=0.025, log2FC=1.5) and E14.5 (P=0.011, log2FC:1.5) in ATRA-treated, whereas methylation TBX22 exon 5 at the CpG site was not significantly different at E16.5 (P=0.808, log2FC=-0.2) between control and ATRA-treated. MSP results showed a similar trend consistent with the MethylRAD-seq results. qPCR showed the change in TBX22 exon 5 expression level negatively correlated with its TBX22 exon 5 methylation level. These results indicate that changes in TBX22 exon 5 methylation might play an important regulatory role during palatal shelf fusion, and may enlighten the development of novel epigenetic biomarkers in the treatment of CP in the future."}

{"project":"Goldhamster2_Cellosaurus","denotations":[{"id":"T1","span":{"begin":277,"end":278},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T2","span":{"begin":581,"end":583},"obj":"CVCL_5M23|Cancer_cell_line|Mesocricetus auratus"},{"id":"T3","span":{"begin":678,"end":683},"obj":"CVCL_ZE35|Undefined_cell_line_type|Mus musculus"},{"id":"T4","span":{"begin":706,"end":709},"obj":"CVCL_0452|Transformed_cell_line|Mus musculus"},{"id":"T5","span":{"begin":753,"end":756},"obj":"CVCL_0452|Transformed_cell_line|Mus musculus"},{"id":"T6","span":{"begin":867,"end":870},"obj":"CVCL_1G78|Spontaneously_immortalized_cell_line|Channa punctata"},{"id":"T7","span":{"begin":989,"end":993},"obj":"CVCL_Y661|Cancer_cell_line|Rattus norvegicus"},{"id":"T8","span":{"begin":998,"end":1001},"obj":"CVCL_1G78|Spontaneously_immortalized_cell_line|Channa punctata"},{"id":"T9","span":{"begin":1124,"end":1125},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T10","span":{"begin":1199,"end":1205},"obj":"CVCL_0238|Cancer_cell_line|Homo sapiens"},{"id":"T11","span":{"begin":1331,"end":1338},"obj":"CVCL_0238|Cancer_cell_line|Homo sapiens"},{"id":"T12","span":{"begin":1378,"end":1380},"obj":"CVCL_8754|Cancer_cell_line|Homo sapiens"},{"id":"T13","span":{"begin":1378,"end":1380},"obj":"CVCL_H241|Cancer_cell_line|Homo sapiens"},{"id":"T14","span":{"begin":1440,"end":1443},"obj":"CVCL_E773|Transformed_cell_line|Homo sapiens"},{"id":"T15","span":{"begin":1521,"end":1523},"obj":"CVCL_6F78|Spontaneously_immortalized_cell_line|Anabas testudineus"}],"text":"Position-dependent correlation between TBX22 exon 5 methylation and palatal shelf fusion in the development of cleft palate.\nDNA methylation is essential for spatiotemporally-regulated gene expression in embryonic development. TBX22 (Chr X: 107667964-107688978) functioning as a transcriptional repressor affects DNA binding, sumoylation, and transcriptional repression associated with X-linked cleft palate. This study aimed to explore the relationship and potential mechanism between TBX22 exon 5 methylation and palatal shelf fusion induced by all-trans retinoic acid (ATRA). We performed DNA methylation profiling, using MethylRAD-seq, after high throughput sequencing of mouse embryos from control (n=9) and ATRA-treated (to induce cleft palate, n=9) C57BL/6J mice at embryonic gestation days(E) 13.5, 14.5 and 16.5. TBX22 exon 5 was hyper-methylated at the CpG site at E13.5 (P=0.025, log2FC=1.5) and E14.5 (P=0.011, log2FC:1.5) in ATRA-treated, whereas methylation TBX22 exon 5 at the CpG site was not significantly different at E16.5 (P=0.808, log2FC=-0.2) between control and ATRA-treated. MSP results showed a similar trend consistent with the MethylRAD-seq results. qPCR showed the change in TBX22 exon 5 expression level negatively correlated with its TBX22 exon 5 methylation level. These results indicate that changes in TBX22 exon 5 methylation might play an important regulatory role during palatal shelf fusion, and may enlighten the development of novel epigenetic biomarkers in the treatment of CP in the future."}

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correlation between TBX22 exon 5 methylation and palatal shelf fusion in the development of cleft palate.\nDNA methylation is essential for spatiotemporally-regulated gene expression in embryonic development. TBX22 (Chr X: 107667964-107688978) functioning as a transcriptional repressor affects DNA binding, sumoylation, and transcriptional repression associated with X-linked cleft palate. This study aimed to explore the relationship and potential mechanism between TBX22 exon 5 methylation and palatal shelf fusion induced by all-trans retinoic acid (ATRA). We performed DNA methylation profiling, using MethylRAD-seq, after high throughput sequencing of mouse embryos from control (n=9) and ATRA-treated (to induce cleft palate, n=9) C57BL/6J mice at embryonic gestation days(E) 13.5, 14.5 and 16.5. TBX22 exon 5 was hyper-methylated at the CpG site at E13.5 (P=0.025, log2FC=1.5) and E14.5 (P=0.011, log2FC:1.5) in ATRA-treated, whereas methylation TBX22 exon 5 at the CpG site was not significantly different at E16.5 (P=0.808, log2FC=-0.2) between control and ATRA-treated. MSP results showed a similar trend consistent with the MethylRAD-seq results. qPCR showed the change in TBX22 exon 5 expression level negatively correlated with its TBX22 exon 5 methylation level. These results indicate that changes in TBX22 exon 5 methylation might play an important regulatory role during palatal shelf fusion, and may enlighten the development of novel epigenetic biomarkers in the treatment of CP in the future."}