Related Experiment Video
Updated: May 31, 2026

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
Published on: June 26, 2020
ASF1A and ATM regulate H3K56-mediated cell-cycle checkpoint recovery in response to UV irradiation
Aruna Battu1, Alo Ray, Altaf A Wani
1Department of Radiology, The Ohio State University, Columbus, OH 43210, USA.
Abstract:
Successful DNA repair within chromatin requires coordinated interplay of histone modifications, chaperones and remodelers for allowing access of repair and checkpoint machineries to damaged sites. Upon completion of repair, ordered restoration of chromatin structure and key epigenetic marks herald the cell's normal function. Here, we demonstrate such a restoration role of H3K56 acetylation (H3K56Ac) mark in response to ultraviolet (UV) irradiation of human cells. A fast initial deacetylation of H3K56 is followed by full renewal of an acetylated state at ~24-48 h post-irradiation. Histone chaperone, anti-silencing function-1 A (ASF1A), is crucial for post-repair H3K56Ac restoration, which in turn, is needed for the dephosphorylation of γ-H2AX and cellular recovery from checkpoint arrest. On the other hand, completion of DNA damage repair is not dependent on ASF1A or H3K56Ac. H3K56Ac restoration is regulated by ataxia telangiectasia mutated (ATM) checkpoint kinase. These cross-talking molecular cellular events reveal the important pathway components influencing the regulatory function of H3K56Ac in the recovery from UV-induced checkpoint arrest.
Related Concept Videos
DNA Damage can Stall the Cell Cycle
DNA Damage Can Stall the Cell Cycle
Restarting Stalled Replication Forks
The Spindle Assembly Checkpoint
Many proteins function together to control the spindle assembly checkpoint. Mutations affecting these proteins may allow cells to proceed into anaphase prematurely, resulting in the...
Separation of Sister Chromatids
At the onset of anaphase, separase, a proteolytic enzyme, is...
Anaphase Promoting Complex

