Sequencing Data Illustrates Polyadenylation of Histone H3.1 mRNA Promotes Cell Transformation by Displacing H3.3 from Gene Regulatory Elements
- Description
Previous study showed that exposure to arsenic, an environmental carcinogen, induces polyadenylation of canonical histone H3.1 mRNA. This study revealed that polyadenylation of H3.1 mRNA increases H3.1 protein, which results in displacement of histone variant H3.3 at active promoters, enhancers, and insulator regions. To investigate global changes in transcription induced by ectopic expression of polyadenylated H3.1 mRNA, RNA sequencing using BEAS-2B cells stably transfected with empty vector, H3.1poly(A), or H3.1Loop were carried out. BEAS-2B cells were stably transfected with pcDNA3.1-NT-Empty or pcDNA3.1-NT-H3.1poly(A) plasmid. For ChIP sequencing, BEAS-2B cells were stably transfected with pcDNA3.1-FLAG-H3.3, and then pcDNA3.1-NT-H3.1poly(A), to obtain BEAS-2B FLAG-H3.3 and BEAS-2B FLAG-H3.3&NT-H3.1poly(A) stable cell lines. The data indicates that H3.3 displacement might be central to carcinogenesis caused by polyadenylation of H3.1 mRNA upon arsenic exposure.
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Free to All
- Instructions
- All sequencing data generated during this study are available at NCBI's Gene Expression Omnibus (GEO) database.
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