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Etoposide induces nuclear re-localisation of AID
Laurens J Lambert1, Simon Walker, Jack Feltham
1Epigenetics Programme, The Babraham Institute, Cambridge, United Kingdom.
Plos One
|December 11, 2013
Summary
Activation-induced cytidine deaminase (AID) relocates to the nucleus during DNA repair after etoposide treatment. This prolonged nuclear presence may enable AID-mediated DNA demethylation for epigenetic reprogramming.
Area of Science:
- Molecular Biology
- Epigenetics
- DNA Repair
Background:
- Activation-induced cytidine deaminase (AID) introduces DNA lesions during B cell activation.
- AID's role in epigenetic reprogramming is suggested but limited by low expression in non-B cells.
- Transient nuclear presence of AID is sufficient for immunoglobulin gene alteration.
Purpose of the Study:
- To investigate the pathway for prolonged nuclear residence of AID.
- To determine if DNA double-strand breaks (DSBs) trigger sustained nuclear localization of AID.
- To explore the potential of AID in epigenetic reprogramming.
Main Methods:
- Etoposide treatment to induce DNA double-strand breaks (DSBs).
- Cell cycle analysis to identify specific phases for AID relocalization.
- Monitoring of AID localization and DNA damage markers (γH2AX).
Main Results:
- AID completely relocalizes to the nucleus 2-6 hours after etoposide treatment during DSB repair.
- AID remains in the nucleus for over 10 hours in live, motile cells.
- Relocalization is cell-cycle dependent, occurring only in G2 phase, and is not directly correlated with γH2AX levels.
Conclusions:
- DSB formation initiates a slow pathway for stable, long-term nuclear localization of AID.
- This pathway may facilitate AID-induced DNA demethylation during epigenetic reprogramming.
- Sustained nuclear AID presence is linked to DNA repair processes and potential epigenetic modifications.
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