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Status |
Public on Apr 17, 2020 |
Title |
HRI activates ATF4 to promote BCL11A transcription and fetal hemoglobin silencing [ChIP-seq] |
Organisms |
Homo sapiens; Mus musculus |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
Through a CRISPR-Cas9 guided loss-of-function screen in human erythroid cells we identified transcription factor ATF4, a known HRI-regulated protein, as a novel γ-globin repressor. ATF4 binds to a BCL11A enhancer to augment promoter contacts, stimulates BCL11A transcription to repress γ-globin expression. Notably, mice deficient for HRI displayed normal Bcl11a levels, suggesting species selective regulation that we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable. This illustrates potential limits of commonly used murine models of globin gene regulation.
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Overall design |
ATF4 ChIP-seq of HUDEP2, Human primary erythroblast and G1E-ER4 cell line
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Contributor(s) |
Huang P |
Citation(s) |
32299090 |
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Submission date |
Jan 20, 2020 |
Last update date |
Apr 19, 2020 |
Contact name |
Peng Huang |
E-mail(s) |
waliays@gmail.com
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Organization name |
Guangzhou Medical University
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Department |
GMU-GIBH Joint School of Life Sciences
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Lab |
Peng Huang
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Street address |
Xinzao, Panyu District
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City |
Guangzhou |
State/province |
Guangdong |
ZIP/Postal code |
511436 |
Country |
China |
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Platforms (2) |
GPL18573 |
Illumina NextSeq 500 (Homo sapiens) |
GPL19057 |
Illumina NextSeq 500 (Mus musculus) |
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Samples (15)
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This SubSeries is part of SuperSeries: |
GSE143963 |
HRI activates ATF4 to promote BCL11A transcription and fetal hemoglobin silencing |
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Relations |
BioProject |
PRJNA602344 |
SRA |
SRP243510 |