Characterization of a human homolog of (6-4)photolyase
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Photolyase
Pyrimidine dimer
Homology
Southern blot
Photolyase
Pyrimidine dimer
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Ultraviolet B radiation (UVBR) damages the DNA of exposed cells, causing dimers to form between adjacent pyrimidine nucleotides. These dimers block DNA replication, causing mutations and apoptosis. Most organisms utilize biochemical or biophysical DNA repair strategies to restore DNA structure; however, as with most biological reactions, these processes are likely to be thermally sensitive. Tadpoles exposed to elevated UVBR at low environmental temperatures have significantly higher rates of mortality and developmental deformities compared with tadpoles exposed to the same levels of UVBR at higher environmental temperatures. We hypothesized that low environmental temperatures impair the primary enzymatic (photolyase) DNA repair pathway in amphibians, leading to the accumulation of DNA damage. To test this hypothesis, we compared DNA repair rates and photolyase gene expression patterns in Limnodynastes peronii. Tadpoles were acutely exposed to UVBR for 1 hr at either 20 or 30°C, and we measured DNA damage and photolyase expression levels at intervals following this exposure. Temperature had a significant effect on the rate of DNA repair, with repair at 30°C occurring twice as fast as repair at 20°C. Photolyase gene expression (6-4 PP and CPD) was significantly upregulated by UVBR exposure, with expression levels increasing within 6 hr of UVBR exposure. CPD expression levels were not significantly affected by temperature, but 6-4 PP expression was significantly higher in tadpoles in the 30°C treatment within 12 hr of UVBR exposure. These data support the hypothesis that DNA repair rates are thermally sensitive in tadpoles and may explain why enigmatic amphibian declines are higher in montane regions where UVBR levels are naturally elevated and environmental temperatures are lower.
Photolyase
Pyrimidine dimer
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Photolyase
Pyrimidine dimer
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Pyrimidine dimer
Thymine
Ultraviolet light
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Photolyase
Pyrimidine dimer
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Ultraviolet light damages DNA by converting two adjacent thymines into a thymine dimer which is potentially mutagenic, carcinogenic, or lethal to the organism. This damage is repaired by photolyase and the nucleotide excision repair system in E. coli by nucleotide excision repair in humans. The work leading to these results is presented by Aziz Sancar in his Nobel Lecture.
Pyrimidine dimer
Photolyase
Nuclease
Thymine
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DNA photolyase represents a phenomenal class of DNA repair enzymes in that it harvests the light energy to repair DNA lesions caused by ultraviolet light. Mother Nature evolves two types of photolyases, one specific for repairing cyclobutane pyrimidine dimers and the other for pyrimidine-(6-4)-pyrimidone photoproducts. Together, these two kinds of DNA photolesions account for the majority of ultraviolet light-induced DNA lesions. So far, the basic chemical steps of the enzyme mechanism of the two classes of photolyases appear to be very similar. Therefore, it will be very interesting to uncover the determinants of the different substrate specificity between the two photolyases. In this review, we focus on the discussion of the photolyase specific for repairing pyrimidine-(6-4)-pyrimidone photoproducts mainly because the research of the cyclobutane pyrimidine dimer photolyase has recently been reviewed quite extensively.
Photolyase
Pyrimidine dimer
Ultraviolet light
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Photolyase
Homology
Coding region
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In their life cycle, plants are exposed to various unfavorable environmental factors including ultraviolet (UV) radiation emitted by the Sun. UV-A and UV-B, which are partially absorbed by the ozone layer, reach the surface of the Earth causing harmful effects among the others on plant genetic material. The energy of UV light is sufficient to induce mutations in DNA. Some examples of DNA damage induced by UV are pyrimidine dimers, oxidized nucleotides as well as single and double-strand breaks. When exposed to light, plants can repair major UV-induced DNA lesions, i.e., pyrimidine dimers using photoreactivation. However, this highly efficient light-dependent DNA repair system is ineffective in dim light or at night. Moreover, it is helpless when it comes to the repair of DNA lesions other than pyrimidine dimers. In this review, we have focused on how plants cope with deleterious DNA damage that cannot be repaired by photoreactivation. The current understanding of light-independent mechanisms, classified as dark DNA repair, indispensable for the maintenance of plant genetic material integrity has been presented.
Photolyase
Pyrimidine dimer
Ultraviolet
Ultraviolet light
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