Uv-induced Dna Damage And Repair A Review Pdf Readers
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- Chromatin and nucleosome dynamics in DNA damage and repair
- Impact of the Circadian Clock on UV-Induced DNA Damage Response and Photocarcinogenesis.
- DNA Damage and Repair in Plants under Ultraviolet and Ionizing Radiations
Chromatin and nucleosome dynamics in DNA damage and repair
Chromatin is organized into higher-order structures that form subcompartments in interphase nuclei. Different categories of specialized enzymes act on chromatin and regulate its compaction and biophysical characteristics in response to physiological conditions. We present an overview of the function of chromatin structure and its dynamic changes in response to genotoxic stress, focusing on both subnuclear organization and the physical mobility of DNA. We review the requirements and mechanisms that cause chromatin relocation, enhanced mobility, and chromatin unfolding as a consequence of genotoxic lesions. An intriguing link has been established recently between enhanced chromatin dynamics and histone loss. Improved live-imaging technologies and experiments that capture long-range contacts between chromosomal domains chromosome conformation capture have shown that the chromatin of yeast, fly, mouse, and human cell nuclei undergoes constant subdiffusive movement and plastic reorganization within interphase nuclei for reviews, see Dekker et al.
Impact of the Circadian Clock on UV-Induced DNA Damage Response and Photocarcinogenesis.
Being sessile, plants are continuously exposed to DNA-damaging agents present in the environment such as ultraviolet UV and ionizing radiations IR. The outcome of the discussion may be helpful in devising future research in the current context. Having sessile nature, plants have to cope with constant exposure of environmental stressors which includes UV-B, ozone, desiccation, rehydration, salinity, low and high temperature, and air and soil pollutants including metals-metalloids. Several chemical mutagens and crosslinking agents e. Apart from severely impacting plant structural, enzymatic and nonenzymatic components, the aforesaid stressors may also negatively threaten plant genomes. Despite the very stable nature of plant genome, nuclear DNA is an inherently unstable molecule and can be damaged spontaneously, metabolically, or by aforesaid stress factors. The overproduction of reactive oxygen species ROS as byproducts of normal cellular metabolism or as a result of abiotic stress conditions leads to DNA damage in the cell [ 2 , 3 ].
DNA Damage and Repair in Plants under Ultraviolet and Ionizing Radiations
Maintenance of genome integrity is a key issue for all living organisms. However, genomes remain extremely stable, thanks to the permanent repair of DNA lesions. The signaling mechanisms of the DDR are quite well conserved between organisms including in plants where they have been investigated into detail over the past 20 years. In this review we summarize the acquired knowledge and recent advances regarding the DDR control of cell cycle progression.
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Global genome nucleotide excision repair removes DNA damage from transcriptionally silent regions of the genome. Relatively little is known about the molecular events that initiate and regulate this process in the context of chromatin. We've shown that, in response to UV radiation—induced DNA damage, increased histone H3 acetylation at lysine 9 and 14 correlates with changes in chromatin structure, and these alterations are associated with efficient global genome nucleotide excision repair in yeast. These changes depend on the presence of the Rad16 protein. Remarkably, constitutive hyperacetylation of histone H3 can suppress the requirement for Rad7 and Rad16, two components of a global genome repair complex, during repair.
Human skin is continuously exposed to environmental DNA damage leading to the accumulation of somatic mutations over the lifetime of an individual. The contributions of these processes to the somatic mutation load in the skin of healthy humans has so far not been accurately assessed because the low numbers of mutations from current sequencing methodologies preclude the distinction between sequencing errors and true somatic genome changes. In this work, we sequenced genomes of single cell-derived clonal lineages obtained from primary skin cells of a large cohort of healthy individuals across a wide range of ages. We report here the range of mutation load and a comprehensive view of the various somatic genome changes that accumulate in skin cells.
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