Setdb1 and Atf7IP form a hetero-trimeric complex that blocks Setdb1 nuclear export
2024
Setdb1 and Atf7IP form a complex that prevents Setdb1 from leaving the nucleus
publication
Evidence: high
Author Information
Author(s): Kariapper Leena, Marathe Ila A., Niesman Ashley B., Suino-Powell Kelly, Min Chook Yuh, Wysocki Vicki H., Worden Evan J.
Primary Institution: Van Andel Institute
Hypothesis
How does Atf7IP interact with Setdb1 to regulate its nuclear localization?
Conclusion
Setdb1 and Atf7IP form a heterotrimeric complex that prevents the nuclear export of Setdb1.
Supporting Evidence
- Setdb1 is critical for silencing retrotransposons in the genome.
- Atf7IP binding stimulates Setdb1's activity and prevents its degradation.
- Alphafold2 models suggest a 1:2 stoichiometry of Setdb1 to Atf7IP.
- Setdb1 and Atf7IP form a stable complex that blocks nuclear export signals.
Takeaway
This study shows that two Atf7IP proteins can attach to one Setdb1 protein, helping keep Setdb1 in the nucleus where it can do its job.
Methodology
The study used biochemical reconstitutions and Alphafold2 predictions to analyze the interaction between Setdb1 and Atf7IP.
Digital Object Identifier (DOI)
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