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Published on: September 20, 2018
H3K27ac mediated SS18/BAFs relocation regulates JUN induced pluripotent-somatic transition
Runxia Lin1,2,3, Ziwei Zhai1,2,3, Junqi Kuang1,2,4,3
1CAS Key Laboratory of Regenerative Biology, Guangzhou Institutes of Biomedicine and Health, Chinese Academy and Sciences, Guangzhou, 510530, China.
Pluripotent-somatic transition (PST) involves rapid chromatin remodeling. The SS18/BAF complex moves from pluripotent to somatic sites, driven by cJUN and H3K27ac, facilitating gene activation during cell fate changes.
Area of Science:
- Developmental Biology
- Epigenetics
- Cell Biology
Background:
- Pluripotent-somatic transition (PST) is a key event in early mammalian development.
- PST serves as a model for understanding cell fate transitions.
Purpose of the Study:
- Investigate chromatin accessibility dynamics (CAD) during JUN-induced PST.
- Elucidate the role of the SS18/BAF chromatin remodeling complex in early PST.
Main Methods:
- Utilized a JUN-induced PST model (8 hours).
- Analyzed chromatin accessibility using ChIP-seq.
- Performed knockdown of Brg1, a core BAF complex component.
- Investigated protein interactions using IP-MS.
Main Results:
- JUN induced opening of 34,661 chromatin sites within 4 hours, activating somatic genes (e.g., Anxa1, Fosl1).
- SS18/BAFs rapidly relocated from pluripotent to AP-1 associated loci.
- Brg1 knockdown impaired chromatin opening and delayed PST.
- H3K27ac, deposited by cJUN, guided SS18/BAFs to AP1 loci, promoting chromatin opening and gene activation.
Conclusions:
- Demonstrated rapid transfer of BAF complexes from pluripotent to somatic loci during PST.
- Revealed a mechanistic aspect of cell fate control involving directed chromatin remodeling.
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