Keronninn Moreno de Lima Bessa
From DNA Repair Lab
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| - | I undergraduated in Biology at the Federal University of Rio Grande do Norte. In 2006, I got my PhD in Biotechnology at the University of Sao Paulo, Brazil. Since november/2006, I am supported by a Postdoctoral Fellowship from FAPESP. | + | I undergraduated in Biology at the Federal University of Rio Grande do Norte. In 2006, I got my PhD in Biotechnology at the University of Sao Paulo, Brazil. Nowadays, I am supported by a Postdoctoral Fellowship from FAPESP. |
Revision as of 14:02, 31 May 2007
I undergraduated in Biology at the Federal University of Rio Grande do Norte. In 2006, I got my PhD in Biotechnology at the University of Sao Paulo, Brazil. Nowadays, I am supported by a Postdoctoral Fellowship from FAPESP.
Project description
Ultraviolet light (UV) generates DNA lesions, cyclobutante pyrimidine dimers (CPDs) and 6-4 pyrimidine-pyrimidone photoproducts being the most frequent ones. These DNA lesions can be removed from the genome by two different DNA repair processes: photoreactivation and nucleotide excision repair (NER). Photoreactivation envolves enzymes named photolyases, which contain chromophores that capture blue photons and use them to repair the UV photoproducts. Interestingly, these enzymes present a high specificity to the target lesion, being classified as CPD-photolyases and 6-4PP-photolyases. Even though photoreactivation has been found widespread in the nature, these enzymes are absent in placental mammals, including humans. In these organisms, repair of UV-induced DNA lesions is performed by NER. Our research work is interested in investigating the effects of CPDs and 6-4PPs on the induction of cellular responses upon UV irradiation. For this purpose, we have constructed adenoviral vectors carrying the marsupial CPD-photolyase and plant 6-4PP-photolyase. By employing these vectors, we have been able to demonstrate that both CPDs and 6-4PPs play important roles in cell death pathways in NER-deficient human fibroblasts, while CPDs are the major signals that lead NER-proficient human cells to death. At this time, we have been employing these recombinant adenoviral vectors for studying the effects of CPDs and 6-4PPs in cellular processes such as DNA replication and RNA transcription, which are inhibited by UV irradiation.
Publications
1. LIMA-BESSA KM, Chiganças V, Stary A, Kannouche P, Sarasin A, Armelini MG, Jacysyn JF, Amarante-Mendes, GP, Cordeiro-Stone M, Cleaver JE, Menck CF. Adenovirus mediated transduction of the human DNA polymerase eta cDNA. DNA Repair, v. 5, p. 925-934, 2006.
2. Armelini MG, Marchetto MC, Muotri AR, LIMA-BESSA KM, Sarasin A, Menck CF. Restoring DNA repair capacity of cells from three distinct diseases by XPD gene-recombinant adenovirus. Cancer Gene Therapy, v. 12, p. 389-396, 2005.
3. LIMA-BESSA KM, Menck CF. Skin cancer: lights on genome lesions. Current Biology, v. 15, p. 58-61, 2005.
4. Martins-Pinheiro M, Galhardo RS, Lage C, LIMA-BESSA KM, Aires KA, Menck CF. Different patterns of evolution for duplicated DNA repair genes in bacteria of the Xanthomonadales group. BMC Evolutionary Biology, v. 4, p. 1-9, 2004.