Use of a UV endonuclease from Micrococcus luteus to monitor the progress of DNA repair in UV-irradiated human cells

Paterson, Malcolm C.; Lohman, P.H.M.; Sluyter, M.L.

doi:10.1016/0027-5107(73)90083-3

Cited by 182 publications

(25 citation statements)

References 20 publications

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“…This is in contrast to repair-proficient cells which are able to perform DNA incision and thus remove ESS . This assay can be used for both in vitro (Strauss et al 1966, Paterson et al . 1973) as well as in vivo (Ganesan 1973 Lett et al .…”

Section: 3 mentioning

confidence: 98%

The Molecular Genetics of the Incision Step in the DNA Excision Repair Process

Rubin

1988

International Journal of Radiation Biology

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This review describes the evolution of research into the genetic basis of how different organisms use the process of excision repair to recognize and remove lesions from their cellular DNA. One particular aspect of excision repair, DNA incision, and how it is controlled at the genetic level in bacteriophage, bacteria, S. cerevisae, D. melanogaster, rodent cells and humans is examined. In phage T4, DNA is incised by a DNA glycosylase-AP endonuclease that is coded for by the denV gene. In E. coli, the products of three genes, uvrA, uvrB and uvrC, are required to form the UVRABC excinuclease that cleaves DNA and releases a fragment 12-13 nucleotides long containing the site of damage. In S. cerevisiae, genes complementing five mutants of the RAD3 epistasis group, rad1, rad2, rad3, rad4 and rad10 have been cloned and analyzed. Rodent cells sensitive to a variety of mutagenic agents and deficient in excision repair are being used in molecular studies to identify and clone human repair genes (e.g. ERCC1) capable of complementing mammalian repair defects. Most studies of the human system, however, have been done with cells isolated from patients suffering from the repair defective, cancer-prone disorder, xeroderma pigmentosum, and these cells are now beginning to be characterized at the molecular level. Studies such as these that provide a greater understanding of the genetic basis of DNA repair should also offer new insights into other cellular processes, including genetic recombination, differentiation, mutagenesis, carcinogenesis and aging.

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Section: 3 mentioning

confidence: 98%

The Molecular Genetics of the Incision Step in the DNA Excision Repair Process

Rubin

1988

International Journal of Radiation Biology

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“…Some of these methods are based on the detection of chromosome breakage (reviewed in [70]) including the Comet assay (see [71][72][73] for review). Other approaches measure the activity of nDNA repair enzymes [74,75] or the amount of damage localized to a plasmid (i.e., to exogenous DNA) that a cell can "reactivate" or repair (socalled host cell reactivation; reviewed in [76]). The common limitation of these methods is that they cannot be used to investigate nDNA repair processes ongoing in the brain in a celltype-specific manner.…”

Section: Nuclear Dna Repairmentioning

confidence: 99%

Accumulation of nuclear DNA damage or neuron loss: Molecular basis for a new approach to understanding selective neuronal vulnerability in neurodegenerative diseases

et al. 2008

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According to a long-standing hypothesis, aging is mainly caused by accumulation of nuclear (n) DNA damage in differentiated cells such as neurons due to insufficient nDNA repair during lifetime. In line with this hypothesis it was until recently widely accepted that neuron loss is a general consequence of normal aging, explaining some degree of decline in brain function during aging. However, with the advent of more accurate procedures for counting neurons, it is currently widely accepted that there is widespread preservation of neuron numbers in the aging brain, and the changes that do occur are relatively specific to certain brain regions and types of neurons. Whether accumulation of nDNA damage and decline in nDNA repair is a general phenomenon in the aging brain or also shows cell-type specificity is, however, not known. It has not been possible to address this issue with the biochemical and molecular-biological methods available to study nDNA damage and nDNA repair. Rather, it was the introduction of autoradiographic methods to study quantitatively the relative amounts of nDNA damage (measured as nDNA single-strand breaks) and nDNA repair (measured as unscheduled DNA synthesis) on tissue sections that made it possible to address this question in a cell-type-specific manner under physiological conditions. The results of these studies revealed a formerly unknown inverse relationship between age-related accumulation of nDNA damage and age-related impairment in nDNA repair on the one hand, and the age-related, selective, loss of neurons on the other hand. This inverse relation may not only reflect a fundamental process of aging in the central nervous system but also provide the molecular basis for a new approach to understand the selective neuronal vulnerability in neurodegenerative diseases, particularly Alzheimer's disease.

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“…Several methods are available for determining the induction and/or repair of DNA photoproducts, including chromatographic (9 -12), enzymatic (13,14), agarose gel electrophoresis (3,15), plasmid host cell reactivation (16) and immunological (17)(18)(19)(20) methods. The immunological method has several advantages over the others.…”

Section: Introductionmentioning

confidence: 99%

Quantitation and Visualization of Ultraviolet‐Induced DNA Damage Using Specific Antibodies: Application to Pigment Cell Biology

Kobayashi

Katsumi

Imoto

et al. 2001

Pigment Cell Research

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The major types of DNA damage induced by sunlight in the scope. This latter method allows us to reconstruct three-diskin are DNA photoproducts, such as cyclobutane pyrimidine mensional images of nuclei containing DNA photoproducts and to simultaneously examine DNA photoproducts and hisdimers (CPDs), (6-4)photoproducts (6-4PPs) and Dewar isotology in multilayered epidermis. Using those techniques, one mers of 6-4PPs. A sensitive method for quantitating and can determine the induction and repair of these three distinct visualizing each type of DNA photoproduct induced by biologtypes of DNA photoproducts in cultured cells and in the skin ically relevant doses of ultraviolet (UV) or sunlight is essential to characterize DNA photoproducts and their biological efexposed to sublethal or suberythematous doses of UV or solar simulated radiation. As examples of the utility of these techfects. We have established monoclonal antibodies specific for niques and antibodies, we describe the DNA repair kinetics CPDs, 6-4PPs or Dewar isomers. Those antibodies allow one to quantitate photoproducts in DNA purified from cultured following irradiation of human cell nuclei and the photoprotective effect of melanin against DNA photoproducts in cultured cells or from the skin epidermis using an enzyme-linked immunosorbent assay. One can also use those specific antibodpigmented cells and in human epidermis. ies with in situ laser cytometry to visualize and measure DNA

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Use of a UV endonuclease from Micrococcus luteus to monitor the progress of DNA repair in UV-irradiated human cells

Cited by 182 publications

References 20 publications

The Molecular Genetics of the Incision Step in the DNA Excision Repair Process

The Molecular Genetics of the Incision Step in the DNA Excision Repair Process

Accumulation of nuclear DNA damage or neuron loss: Molecular basis for a new approach to understanding selective neuronal vulnerability in neurodegenerative diseases

Quantitation and Visualization of Ultraviolet‐Induced DNA Damage Using Specific Antibodies: Application to Pigment Cell Biology

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