Annotated Bibliographies Nicolle A. Rosa Mercado UPR Cayey Biology Department Biol. 3095 Fall semester RISEFirst Anntotated BibliographyOctober 12, 2012Kunz B, Dando P, Grice D, Mohr P, Schenk P, and Cahill D. 2008. UV-Induced DNA DamagePromotes Resistance to the Biotrophic Pathogen Hyaloperonospora parasitica in Arabidopsis.American Society of Plant Biologists 148: 1021-1031.This study evaluates the possibility that ultra-violet (UV) rays may contribute to plant immunitydiseases. The investigators suspect that UV rays indirectly help the plant to create a resistance topathogens such as Hyaloperonospora parasitica. They show that cyclobutane pyrimidine dimers(CPDs) and 6-4 photoproducts (6-4PPs) have a very important role in the ability of the plants todevelop pathogen resistance. It was discovered that plants that where exposed to low levels of UVBradiation for 26 days accumulated great amount of DNA damage. It is also proposed that other typesof DNA damage might induce resistance to pathogens that may be harmful to Arabidopsis thalianaand other types of plants. These researchers have discarded the possibility of UV rays activatingsystemic acquired resistance (SAR). They concluded that DNA that has been damaged by ultra-violet rays activate defense mechanisms that fight against pathogens harmful to the plants. It is avery interesting fact that something that can be so perilous to humans is actualy able to help otherorganisms when exposed to the correct amount.Second Annotated BibliographyOctober 19, 2012Oh K, Bustin M, Mazur S, Appellac E, Kraemer K. 2010. UV-induced histone H2AXphosphorylation and DNA damage related proteins accumulate and persist in nucleotide excisionrepair-deficient XP-B cells. DNA Repair 10: 5-15In this article, researchers evaluate the effect of DNA damage on XP-B cells associated with theprimordial stages of nucleotide excision repair (NER). Exposure to ultra-violet rays does notdirectly cause DNA double stranded breaks (DSB) . These breaks are considered deformities inthe genome that may be very harmful when formed in proliferating cells. This study verifies thepersistence of DNA damage related (DDR) proteins after UV exposure. This exposure causesDNA damage, and the phosphorylation of histone H2AX. The phosphorylation of histone H2AX isdue to DNA damage involved with the development of DSB. Results show the complexity of DNAdamage processing after UV exposure in normal cells and cells with defective DNA repairmechanisms. They also demonstrate that the DDR pathways may be activated by UV even whenthere is a lack of NER and that localized or uniform UV treatment results in the phosphorylation ofseveral DDR proteins.It is very important to understand how DDR proteins work when exposed toanother hazardous feature.Third Annotated BibliographyNovember 2, 2012
Nijhofa, Joanne W; Muldera, Aat M, Speksnijderb, Ewoud N, Hoogervorstb, Esther M,Mullendersc, Leon H, De Gruijl, Frank R. 2007. Growth stimulation of UV-induced DNA damageretaining epidermal basal cells gives rise to clusters of p53 overexpressing cells. DNA Repair6:1642-1650This investigation studies how ultra violet (UV) radiation affects cyclobutane pyrimidine dimers(CPDs) and (6-4) photoproducts ((6-4) PPs). It is hypothesized that CPDs and (6-4) PPs can formclusters of cells that may lead to skin carcinomas. Cells that accumulate CPDs are known as CPD-retaining basal cells (CRBCs). CRBCs may form tumors due to damaged DNA. DNA damage leadsto the activation of the wild type p53 protein. The presence of this protein may cause apoptosis. Theinvestigators wanted to know if the CRBCs are precursors of the p53 patches. The methodology ofthis investigation consisted of exposing mice to UV radiation and treating them with TPA.Afterwards they extracted skin tissue and applied antibodies. These tissue cells were observedunder a microscope to obtain the quantity of CPD-retaining cells. The methods used by theseinvestigators are very reliable and relatively simple for any other scientist interested in repeatingtheir experiment.The results of their experiment suggest that the CRBCs were activated by lowlevel of ultra violet radiation. It was also demonstrated that CRBCs are related to the creation of p53clusters after the applications of 12-O-tetradecanoylphorbol-13-acetate (TPA).