Keronninn Moreno de Lima Bessa

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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. Nowadays, I am supported by a Postdoctoral Fellowship from FAPESP.

Research project

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 involves 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. So far, 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.


1. LIMA-BESSA KM, Armelini MG, Chiganças V, Jacysyn JF, Amarante-Mendes GP, Sarasin A, Menck CF.CPDs and 6-4PPs play different roles in UV-induced cell death in normal and NER-deficient human cells. DNA Repair, v. 7, n. 2, p. 303-312, 2008.

2. Armelini MG, LIMA-BESSA KM, Marchetto MC, Muotri AR, Chiganças V, Leite RA, Carvalho H, Menck CF. Exploring DNA damage responses in human cells with recombinant adenoviral vectors. Hum Exp Toxicol, v. 26, n. 11, p. 899-906, 2007.

3. Menck, CF, Armelini, MG, LIMA-BESSA KM.On the search for skin gene therapy strategies of xeroderma pigmentosum disease. Current Gene Therapy, v. 7, n. 3, p. 163-174, 2007.

4. 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.

5. LIMA-BESSA KM, Menck CF. Skin cancer: lights on genome lesions. Current Biology, v. 15, p. 58-61, 2005.

6. 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.

7. 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.

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