1) The document discusses three annotated bibliographies about research on the effects of UV radiation on DNA and plant/human cells. 2) The first study shows that UVB radiation can induce DNA damage in plants that helps them develop resistance to pathogens. The second study examines how DNA damage response proteins accumulate in cells defective in DNA repair after UV exposure. 3) The third study investigates how UV-induced DNA lesions like CPDs can form clusters of cells that may lead to skin cancer, and suggests clusters of p53-overexpressing cells originate from CRBCs activated by low-level UV radiation.

1. Annotated Bibliographies
Nicolle A. Rosa Mercado
UPR Cayey
Biology Department
Biol. 3095 Fall semester
RISE
First Anntotated Bibliography
October 12, 2012
Kunz B, Dando P, Grice D, Mohr P, Schenk P, and Cahill D. 2008. UV-Induced DNA Damage
Promotes 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 immunity
diseases. The investigators suspect that UV rays indirectly help the plant to create a resistance to
pathogens 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 to
develop pathogen resistance. It was discovered that plants that where exposed to low levels of UVB
radiation for 26 days accumulated great amount of DNA damage. It is also proposed that other types
of DNA damage might induce resistance to pathogens that may be harmful to Arabidopsis thaliana
and other types of plants. These researchers have discarded the possibility of UV rays activating
systemic 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 a
very interesting fact that something that can be so perilous to humans is actualy able to help other
organisms when exposed to the correct amount.
Second Annotated Bibliography
October 19, 2012
Oh K, Bustin M, Mazur S, Appellac E, Kraemer K. 2010. UV-induced histone H2AX
phosphorylation and DNA damage related proteins accumulate and persist in nucleotide excision
repair-deficient XP-B cells. DNA Repair 10: 5-15
In this article, researchers evaluate the effect of DNA damage on XP-B cells associated with the
primordial stages of nucleotide excision repair (NER). Exposure to ultra-violet rays does not
directly cause DNA double stranded breaks (DSB) . These breaks are considered deformities in
the genome that may be very harmful when formed in proliferating cells. This study verifies the
persistence of DNA damage related (DDR) proteins after UV exposure. This exposure causes
DNA damage, and the phosphorylation of histone H2AX. The phosphorylation of histone H2AX is
due to DNA damage involved with the development of DSB. Results show the complexity of DNA
damage processing after UV exposure in normal cells and cells with defective DNA repair
mechanisms. They also demonstrate that the DDR pathways may be activated by UV even when
there is a lack of NER and that localized or uniform UV treatment results in the phosphorylation of
several DDR proteins.It is very important to understand how DDR proteins work when exposed to
another hazardous feature.
Third Annotated Bibliography
November 2, 2012

2. 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 damage
retaining epidermal basal cells gives rise to clusters of p53 overexpressing cells. DNA Repair
6:1642-1650
This 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 form
clusters 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 leads
to the activation of the wild type p53 protein. The presence of this protein may cause apoptosis. The
investigators wanted to know if the CRBCs are precursors of the p53 patches. The methodology of
this 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 observed
under a microscope to obtain the quantity of CPD-retaining cells. The methods used by these
investigators are very reliable and relatively simple for any other scientist interested in repeating
their experiment.The results of their experiment suggest that the CRBCs were activated by low
level of ultra violet radiation. It was also demonstrated that CRBCs are related to the creation of p53
clusters after the applications of 12-O-tetradecanoylphorbol-13-acetate (TPA).