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Status |
Public on Aug 23, 2020 |
Title |
HDAC3 ensures stepwise epidermal stratification via NCoR/SMRT-reliant mechanisms independent of its histone deacetylase activity (HDAC3_KLF4_ChIPseq) |
Organism |
Mus musculus |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
Chromatin modifiers play critical roles in epidermal development, but the functions of histone deacetylases in this context are poorly understood. We find that the Class I HDAC, HDAC3, is expressed broadly in embryonic epidermis, and is required for its orderly stepwise stratification. Stability of HDAC3 protein in vivo is reliant on NCoR and SMRT, which function redundantly in epidermal development. However, point mutations in the NCoR and SMRT Deacetylase Activating Domains, which are required for HDAC3’s enzymatic function, permit normal stratification, indicating that HDAC3’s roles in this context are independent of its histone deacetylase activity. HDAC3 functions both in conjunction with, and independent of, KLF4 to repress premature expression of different sets of terminal differentiation genes and suppresses expression of inflammatory cytokines through a RelA-dependent mechanism. These data identify HDAC3 as a hub coordinating multiple aspects of epidermal barrier acquisition.
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Overall design |
Examination of HDAC3 and KLF4 genomic binding sites in E18.5 embryonic epidermis
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Contributor(s) |
Millar SE, Szigety KM |
Citation(s) |
32467224 |
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Submission date |
Sep 10, 2019 |
Last update date |
Aug 22, 2024 |
Contact name |
Sarah E Millar |
E-mail(s) |
sarah.millar@mssm.edu
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Organization name |
Icahn School of Medicine at Mount Sinai
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Department |
Developmental, Cell and Regenerative Biology
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Street address |
Icahn Building, Floor 13 Room 020C, 1425 Madison Ave
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City |
New York |
State/province |
NY |
ZIP/Postal code |
10029 |
Country |
USA |
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Platforms (1) |
GPL13112 |
Illumina HiSeq 2000 (Mus musculus) |
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Samples (3) |
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This SubSeries is part of SuperSeries: |
GSE137235 |
HDAC3 ensures stepwise epidermal stratification via NCoR/SMRT-reliant mechanisms independent of its histone deacetylase activity |
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Relations |
BioProject |
PRJNA564839 |
SRA |
SRP221292 |