Abstract
Genomic integrity is constantly insulted by solar ultraviolet (UV) radiation. Adaptative cellular mechanisms called DNA damage responses comprising DNA repair, cell cycle checkpoint, and apoptosis, are believed to be evolved to limit genomic instability according to the photoperiod during a day. As seen in many other key cellular metabolisms, genome surveillance mechanisms against genotoxic UV radiation are under the control of circadian clock systems, thereby exhibiting daily oscillations in their catalytic activities. Indeed, it has been demonstrated that nucleotide excision repair (NER), the sole DNA repair mechanism correcting UV-induced DNA photolesions, and ataxia–telangiectasia-mutated and Rad3-related (ATR)-mediated cell cycle checkpoint kinase are subjected to the robust control of the circadian clock. The molecular foundation for the circadian rhythm of UV-induced DNA damage responses in mammalian cells will be discussed.
Highlights
Everlasting day-night cycles and the accompanying environmental oscillations have placed evolutionary pressure on most organisms on Earth
Rhythmic oscillations in physiology and behavior with a period close to 24 h are called circadian rhythms, which are generated by the cell-autonomous molecular clock operating virtually in every single cell [2]
The mammalian molecular clock system is a conserved transcriptional and translational autoregulatory feedback loop through the concerted action of the heterodimeric transcription activator’s CLOCK-BMAL1 complex, which induces the transcription of target genes that contain E-box elements (CACGTG) in their promoter and/or enhancer regions
Summary
Pyrimidine–pyrimidone (6-4) photoproducts (6-4PP) [6] Because these photolesions can interfere with pivotal DNA metabolisms, including replication and transcription, if Biomolecules 2021, 11, 715. To stimulate the kinase activity of ATR, a common DNA structure consisting at least partly of single-stranded DNA covered with replication protein A (RPA) is a prerequisite. This structure can be generated during the NER process as an intermediate and can serve as a platform for the recruitment of ATR-interacting protein (ATRIP), which facilitates ATR recruitment to the damaged site. The recent findings on the circadian rhythm of NER and the ATR pathways and possible crosstalk between the two systems will be discussed to shed light on the role of the circadian clock system in UV-evoked DNA damage responses and to translate it into clinical application for human health
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