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Checkpoint kinases regulate the circadian clock after DNA damage by influencing chromatin dynamics
Checkpoint kinases influence the body’s internal clock after DNA damage by changing how DNA is packaged
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Abstract
CHK1/2 are essential for maintaining robust circadian rhythms during DNA damage stress.
- Deletion of chk1/2 disrupted the rhythmic transcription of the clock gene frq under DNA damage stress.
- CHK1/2 regulate chromatin structure by interacting with the transcription activator White Collar complex (WCC) at the frq promoter.
- Phosphorylation of H3T11 by CHK1/2 promotes H3 acetylation, particularly H3K56 acetylation, to counteract histone variant H2A.Z deposition.
- A genome-wide correlation exists between H3T11 phosphorylation and H3K56 acetylation, specifically at the frq promoter dependent on CHK1/2.
- CHK1/2 are linked to the rhythmic transcription of metabolic and DNA repair genes during DNA damage.
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