Deacetylase activity-independent transcriptional activation by HDAC2 during TPA-induced HL-60 cell differentiationopen access
- Authors
- Jung, Hyeonsoo; Kim, Ji-Young; Kim, Kee-Beom; Chae, Yun-Cheol; Hahn, Yoonsoo; Kim, Jung-Woong; Seo, Sang-Beom
- Issue Date
- Aug-2018
- Publisher
- PUBLIC LIBRARY SCIENCE
- Citation
- PLOS ONE, v.13, no.8
- Journal Title
- PLOS ONE
- Volume
- 13
- Number
- 8
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/1877
- DOI
- 10.1371/journal.pone.0202935
- ISSN
- 1932-6203
- Abstract
- The human myeloid leukemia cell line HL-60 differentiate into monocytes following treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA). However, the mechanism underlying the differentiation of these cells in response to TPA has not been fully elucidated. In this study, we performed ChIP-seq profiling of RNA Pol II, HDAC2, Acetyl H3 (AcH3), and H3K27me3 and analyzed differential chromatin state changes during TPA-induced differentiation of HL-60 cells. We focused on atypically active genes, which showed enhanced H3 acetylation despite increased HDAC2 recruitment. We found that HDAC2 positively regulates the expression of these genes in a histone deacetylase activity-independent manner. HDAC2 interacted with and recruited paired box 5 (PAX5) to the promoters of the target genes and regulated HL-60 cell differentiation by PAX5-mediated gene activation. Taken together, these data elucidated the specific-chromatin status during HL-60 cell differentiation following TPA exposure and suggested that HDAC2 can activate transcription of certain genes through interactions with PAX5 in a deacetylase activity-independent pathway.
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- Appears in
Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
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