Journal
MOLECULAR CELL
Volume 29, Issue 2, Pages 232-242Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2007.11.020
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Funding
- NHLBI NIH HHS [T32 HL007150, T32 HL 007150-31] Funding Source: Medline
- NIDDK NIH HHS [DK 54937, R01 DK054937, R01 DK058044-05A1, R01 DK054937-08, R37 DK058044, R01 DK054937-07, DK 58044, R01 DK058044-06, R01 DK058044] Funding Source: Medline
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Enhancers can regulate designate promoters over long distances by forming chromatin loops. Whether chromatin loops are lost or reconfigured during gene repression is largely unexplored. We examined the chromosome conformation of the Kit gene that is expressed during early erythropoiesis but is downregulated upon cell maturation. Kit expression is controlled by sequential occupancy of two GATA family transcription factors. In immature cells, a distal enhancer bound by GATA-2 is in physical proximity with the active Kit promoter. Upon cell maturation, GATA-1 displaces GATA-2 and triggers a loss of the enhancer/promoter interaction. Moreover, GATA-1 reciprocally increases the proximity in nuclear space among distinct downstream GATA elements. GATA-1-induced transitions in chromatin conformation are not simply the consequence of transcription inhibition and require the cofactor FOG-1. This work shows that a GATA factor exchange reconfigures higher-order chromatin organization, and suggests that de novo chromatin loop formation is employed by nuclear factors to specify repressive outcomes.
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