Genome Organization with DNA Repair and Damage Caused by UV Light

Sajna Bonsle^*
*Correspondence: Sajna Bonsle, Department of Biotechnology, University of Kerala, Trivandrum, Kerala, India, Email:

Introduction

Genome organization plays a critical role in the response to UV-induced DNA damage and repair processes. UV radiation, particularly in the form of UV-B and UV-C wavelengths, can cause a variety of DNA lesions, such as pyrimidine dimers and DNA crosslinks. These lesions disrupt the normal structure and integrity of the genome, leading to potential mutagenic and carcinogenic effects. However, the organization of the genome, including chromatin structure and nuclear architecture, influences the accessibility of DNA repair machinery to the damaged sites and the efficiency of repair processes. The organization of the genome within the nucleus is not random but rather highly regulated. Chromatin, the complex of DNA and associated proteins, is organized into higher-order structures, including nucleosomes, chromatin loops, and Topologically Associated Domains (TADs). These structures play a crucial role in gene expression, DNA replication, and DNA repair. UV-induced DNA damage can affect the local chromatin structure, leading to changes in nucleosome positioning and accessibility of repair proteins to the damaged DNA.

Description

Nucleotide Excision Repair (NER) is the primary pathway involved in repairing UV-induced DNA damage. NER recognizes and removes the damaged DNA lesions, followed by DNA synthesis and ligation to restore the original DNA sequence. The efficiency of NER is influenced by the chromatin structure and DNA packaging. Access to the damaged sites within tightly compacted chromatin regions can be limited, making the repair process less efficient. Conversely, regions of open chromatin and transcriptionally active genes may facilitate more accessible DNA lesions, resulting in more effective repair. In addition to chromatin structure, genome organization at larger scales, such as TADs and nuclear compartments, can impact UV-induced DNA damage and repair. TADs are self-interacting genomic regions that play a role in gene regulation and DNA repair. UV-induced DNA damage can disrupt TAD boundaries and alter the interactions between DNA repair factors and the damaged sites. Changes in TAD organization can affect the efficiency and accuracy of repair processes [1,2].

Furthermore, the spatial organization of the nucleus and nuclear compartments can influence UV-induced DNA damage repair. Nuclear compartments, such as the nucleolus and nuclear speckles, are involved in various cellular processes, including DNA repair. The relocalization of repair factors to these nuclear compartments upon UV irradiation can enhance repair efficiency and facilitate the recruitment of additional repair proteins to the damaged sites. In summary, genome organization, including chromatin structure, TAD organization, and nuclear compartments, plays crucial role in the response to UV-induced DNA damage and repair. The accessibility of DNA lesions to repair machinery and the efficiency of repair processes are influenced by the organization of the genome. Understanding the relationship between genome organization and UV-induced DNA damage repair can provide insights into the mechanisms underlying DNA repair and contribute to the development of strategies to enhance repair efficiency and minimize the mutagenic effects of UV radiation [3-5].

Conclusion

Understanding the intricate relationship between genome organization and UV-induced DNA damage and repair has important implications in various fields, including cancer biology and environmental health. Deregulation of genome organization and impaired DNA repair processes can contribute to the accumulation of UV-induced mutations and increase the risk of developing skin cancers. Strategies aimed at modulating genome organization or enhancing DNA repair efficiency may have therapeutic potential in preventing or treating UV radiation-associated diseases. In conclusion, genome organization plays a significant role in the response to UV-induced DNA damage and repair. The organization of chromatin, the spatial arrangement of DNA within the nucleus, and the temporal regulation of DNA replication and repair processes all influence the accessibility of DNA lesions and the efficiency of repair mechanisms. Further research into the interplay between genome organization and UV-induced DNA damage and repair will deepen our understanding of the underlying mechanisms and may lead to novel approaches for preventing and treating UV-related diseases.

Acknowledgement

None.

Conflict of Interest

None.

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