My note on paper: RNF8- and RNF168-dependent degradation of KDM4A/JMJD2A triggers 53BP1 recruitment to DNA damage sites

Paper: RNF8- and RNF168-dependent degradation of KDM4A/JMJD2A triggers 53BP1 recruitment to DNA damage sites
(doi:10.1038/emboj.2012.47)

Recruitment of 53BP1 relies on
1. ubiquitination activity of RNF8-RNF168
2. methylation of histone H4 on K20
----
Research gap:
No molecular detail on how 53BP1 get access to the methylated histone H4
----
Findings:
1. JMJD2A(KDM4A) binds the methylated histone
2. JMJD2A is degraded by proteasome through the RNF8 mechanism
3. Abnormal expression, JMJD2 hinds the methylated H4 from 53BP1on the damage site  - reflect JMJD2A mask the accessibility  of 53BP1 to methylated H4
4. Lacking of RNF8+RNF168 -- plus reduce level of JMJD2A + JMJD2B - rescue 53BP1 foci
----
Conclusion:
RNF8 control the accessibility of 53BP1 through the degradation of JMJD2A, by adding the ubiquitin tag on it
----
Remarks:
Cell line use: U2OS (Human osteosarcoma cells)