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Profiling of histone 3 lysine 27 acetylation reveals its role in the chronic DSS-induced colitis mouse model

ABSTRACT: To investigate whether the H3K27ac is involved in the development of inflammatory bowal disease. We established dextran sulfate sodium (DSS)-induced chronic colitis and performed RNA-sequencing and Chromatin Immunoprecipitation followed by NGS sequencing for H3K27ac in the mice colon tissues. We find that the global H3K27ac distribution in colon tissue had no significant difference, while on the typical-enhancers specific in the DSS group, H3K27ac signals were significantly enriched when compared with the control. Furthermore, we identified 89 candidate genes which represented the susceptible genes to H3K27ac change and predicted transcription factors (TFs) upon the DSS treatment. Collectively, our study revealed that H3K27ac increase on special typical-enhancers is possibly related to the development of intestinal inflammation by up-regulating adjacent gene expression and shifting TFs networks.

ORGANISM(S): Mus musculus

PROVIDER: GSE129454 | GEO | 2020/01/18

REPOSITORIES: GEO

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Histone 3 lysine 27 acetylation profiling reveals its role in the chronic DSS-induced colitis mouse model [RNA-seq]

Project description:To investigate whether the H3K27ac is involved in the development of inflammatory bowal disease. We established dextran sulfate sodium (DSS)-induced chronic colitis and performed RNA-sequencing and Chromatin Immunoprecipitation followed by NGS sequencing for H3K27ac in the mice colon tissues. We find that the global H3K27ac distribution in colon tissue had no significant difference, while on the typical-enhancers specific in the DSS group, H3K27ac signals were significantly enriched when compared with the control. Furthermore, we identified 89 candidate genes which represented the susceptible genes to H3K27ac change and predicted transcription factors (TFs) upon the DSS treatment. Collectively, our study revealed that H3K27ac increase on special typical-enhancers is possibly related to the development of intestinal inflammation by up-regulating adjacent gene expression and shifting TFs networks.

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