Caffeine Inhibited Saccharomyces Cerevisiae 's Dna Repair System

UV radiation, such as that from the sun can be very harmful. It has been shown to cause many different mutations within cells, leading to issues for the organism such as death or disease. One of the most prevalent sources of UV radiation for humans is the sun. It’s very important for us to know the extent of cellular damage that can be caused by this radiation, as to know how harmful the sun’s rays are to us as humans. One way that the damage caused by the suns radiation can be tested is through the model organism yeast. For this lab, we exposed two different strains of yeast to UV radiation to test its affects. One strain was able to self-repair, while one was genetically altered so that it could not. Observations were recorded at

On December 10, 2015, three profound individuals received the Nobel Prize in chemistry for their work on DNA repair systems. Paul Modrich, Thomas Lindahl, and Aziz Sancar studied how the cell repairs and protects the information held in its DNA; specifically, Paul Modrich focused on DNA mismatch repair. Since DNA constantly replicates, damage and incorrect pairings are expected, but enzymes watch over DNA as it replicates and repair any errors that occur. In the mismatch repair system, enzymes find the mismatch in the copy of DNA, cut the incorrect section out, and replace it with the correct sequence. Paul Modrich’s study of the mismatch repair system has provided the medical field with important information regarding cancer growth and the possibility of a cure.

- Why does Ultra Violet light at 260nm cause the most damage to DNA? Does damage caused by UV light affect DNA in both prokaryotic and eukaryotic cells alike?

The effects of EMR upon biological systems depend both upon the radiation's power and its frequency. For EMR of visible frequencies or lower the damage done to cells and other materials is determined mainly by power and caused primarily by heating effects from the combined energy transfer of many photons. By contrast, for ultraviolet and higher frequencies chemical materials and living cells can be further damaged beyond that done by simple heating, since individual photons of such high frequency have enough energy to cause direct molecular

DNA can be damaged in two ways by radiation; directly broken by the radiation, or the radiation will ionize water molecules in the body and the free radical interacts with DNA strands and breaks them [1]. Even though repair is possible, it may be harder if both strands of the DNA are broken rather than just one, resulting in cell death or permanent damage to the DNA. Radiation is an important factor when planning for longer manned trips such as to Mars. Mars has no global magnetic field, and a very thin atmosphere so it cannot provide sufficient protection from radiation at the surface of the planet [2]. Earth’s multiple layers in its atmosphere blocks out most of the lethal forms of radiation.

Studies have shown that hydroxyl radical is responsible for oxidative DNA damage. Hydroxyl radicals come from the reaction between ascorbate (vitamin C), uranyl acetate, and hydrogen peroxide as illustrated in scheme 1 . The mechanism of DNA damage begins when the reaction between uranyl acetate and ascorbate (vitamin C) makes plasmid relaxation in pBluescript DNA. pBluescript DNA is a phagemid which includes many advantageous sequences for utilizing cloning with bacteriophage. The rate of DNA strand breaks multiply when the reaction between ascorbate (vitamin C), and uranyl acetate increase. In addition, hydrogen peroxide is the end product when there is a reaction between uranyl ion and ascorbate. DNA damage can happen

Although DNA remains mostly stable, it is constantly subject to chemical modification from a variety of different sources. Numerous forms of DNA damage have been identified resulting from different factors such as alkylating agents, hydrolytic deamination, free radicals, and mismatching base pairs. Alkylating agents cause mutations of legitimate bases, transforming them in to either a non-coding or lethal lesion in the DNA. Hydrolytic deamination changes on base on the DNA double helix into another. (Sinha & Häder, 2002) Oxygen radicals are generated during cellular production of O2 gas is known to either attack the bases of DNA (A, T C, or G) or the Deoxyribose to damage the DNA bases or break strands. (Marnett, 2000) DNA remains under threat by other cellular factors, but it does have certain mechanisms in place to repair certain

Hydroxyl radical, product of the Fenton reaction, the most destructive species among oxygen radicals, is highly toxic and capable of attacking DNA, and oxidizing guanine bases resulting in the formation of mutagenic 8-hydroxy-2 '-deoxyguanosine (8-oxo-2dG) lesions. Among the purine and pyrimidine bases of DNA, guanine is the most sensitive base to oxidation. During an oxidative

In addition, it is also shown that γ-irradiation causes DNA lesions that are not well repaired in HGPS cells4. As the study shows, molecular details about how repair proteins and checkpoints are responsible for DNA repair mechanism are still unknown4. To unravel the complications in deficiency of DNA repair mechanisms and their relationship with H3K9me3, immunofluorescence staining and confocal microscopy were carried out and it was found that γ-H2AX/53BP1 foci were associated with regions enriched with H3K9me34. Moreover, to analyze the hypothesis that H3K9me3 poses a barrier for defective DNA repair, SUV39 was knocked down by siRNA and it was revealed that DNA damage foci decreased significantly which proved the hypothesis tested4. In addition to this hypothesis, it should be also proven if SUV39H1 levels directly contribute to deficiency of DNA repair and checkpoint response proteins in progeria. For this purpose, levels of SUV39H1mRNA in cells with ectopic progerin were analyzed and it was concluded that SUV39H1 levels were significantly increased in mouse embryonic fibroblasts (MEFs) in comparison to the wild type control4. Based on previous hypotheses, it can be implied that since H3K9me3 is mainly catalyzed by SUV39H1 methyltransferase, levels of H3K9me3 must be higher in Zmpste24 - / -

Previous researchers found that irradiation from medium-pressure (MP) UV lamps (polychromatic) was more effective to inactivate adenovirus than UV 254 nm emitting low-pressure (LP) UV lamp (monochromatic). The reason seems to be due to the damage to viral capsid protein by the MP UV emission. In addition, there is different resistance to UV light among adenovirus serotypes1. Although numerous

The human body is made up of approximately 80% water (H2O) molecules. When radiation strikes a water molecule it causes radiolysis. Radiolysis is the disassociation of water into an ion pair (H+ and OH-) and two free radicals (H* and OH*). Free radicals are highly reactive, unstable and capable of disrupting bonds and causing deoxyribonucleic (DNA) damage. DNA is the molecule that holds the genetic information needed for cell duplication and is considered the target molecule for radiobiology. Ionization is the removal of an orbiting electron from an atom. There are two effects of ionizing radiation on a cell: indirect and direct. Direct action occurs when DNA is hit by ionizing radiation. Indirect action occurs when free radicals transfer

Nuclear radiation such as X-rays and UV rays, have the ability to penetrate the nucleus and

On Earth, the layers of atmosphere shield us from most of the radiation that could ever reach us but not all radiation is filtered like UV radiation. If there was no atmosphere, the high-energy particles can rip through the DNA’s links and cause mutations (usually in the form of cancer). When a high-energy particle affects the DNA/RNA or molecules, it can rip apart links or chains in the DNA/molecules. [3] The links that ripped apart a DNA can cause cancer and can affect chromosomes in the process. This process eventually leads to death if the DNA/RNA or cell is unable to repair the damage bonds. Exposure radiation can cause either an acute or chronic radiation poisoning. [3] Acute radiation is simply one large exposure to radiation either from high-energy/ionized or cosmic rays. Instead of having one large exposure of radiation, chronic radiation is having small doses over time, hence the

Maintenance of genomic integrity is crucial for cell survival in resistance to endogenous and exogenous environmental insults to the genetic material. Multiple DNA repair pathways coordinate the response to such genotoxins and protect our genome [1]. Endogenous insults may be generated as a byproduct of cellular metabolism in the form of reactive oxygen species or during physiological processes such as meiotic recombination, mating-type switching in yeasts, V(D)J recombination and DNA replication-transcription collision [2-5]. Exogenous stresses include hypoxia, radiation and dietary carcinogens [6, 7]. Depending on the nature of damage to the DNA structure which, may range from breaks in phosphodiester bonds such

Modification of damaged DNA seems to be an understudied subject, there is much to understand on the restoration of DNA damage, repair and DNA methylation. Genomic DNA can be modified by methylation but much of it is affected on a gene when silenced. When epigenetic modification has been implicated with cancer and aging it causes DNA methylation to also have an impact on the double strand of DNA analysis. Modification as such provoke deteriorating changes like aging found in multicellular organisms and DNA damage may magnify biochemical pathways that regulate a cells growth or control DNA replication with DNA repair. In the article “DNA Damage, Homology-Directed Repair, and DNA Methylation” written by Concetta Cuozzo, Antonio Porcellini, Tiziana Angrisano, et al. they hypothesize how DNA damage and gene silencing may induce a DNA double-strand break within a genome as well as when DNA methylation is induced by homologous recombination that it may somewhat mark its reparation through a DNA segment and protect its cells against any unregulated gene expression that may be followed by DNA damage. The experiments used to demonstration how gene conversion can modify methylation pattern of repaired DNA and when that occurs methylation is able to silence the recombined gene. When exploring the molecular mechanisms that link DNA damage and the silencing gene then there is an induced double strand break that can be found at a specific location or DNA sequence in where the