58º Congresso Brasileiro de Genética
Resumos do 58o Congresso Brasileiro de Genética • 11 a 14 de setembro de 2012
Rafain Palace Hotel e Convention Center • Foz do Iguaçu • PR • Brasil
www.sbg.org.br - ISBN 978-85-89109-06-2
44
XPC protein regulates the expression and
localization of parp-1AFTER Oxidative stress
Monte, JFS1; de Melo, JTA1,2; Pinheiro, SN1; Lajus, TBP1,3; Lima-Bessa, KM1; Agnez-Lima, LF1
1
Universidade Federal do Rio Grande do Norte - Departamento de Biologia Celular e Genética; 2Universidade Federal do
Rio Grande do Norte - Faculdade de Ciências da Saúde do Trairi; 3Liga Norte - Riograndense Contra o Câncer - LNRCC.
[email protected]
Keywords: NER, XPC, PARP-1, expression, localization.
Most of the knowledge about the Nucleotide Excision Repair (NER) functions comes from studies with ultraviolet
light (UV). However, even though unrepaired UV-induced DNA damages are related to mutagenesis, cell death
and tumorigenesis events, they do not justify phenotypes as neurodegeneration and internal tumors observed in
patients with syndromes related to NER deficiency, as Cockayne Syndrome (CS) and Xeroderma Pigmentosum (XP).
Moreover, new insights have been pointing to a role of NER in the repair of oxidative DNA damage, the main
substrate to Base Excision Repair (BER). In order to address the impact of the NER deficiency in the BER capacities,
we have treated NER-proficient and NER-deficient cells with H2O2, and investigated both the expression levels and
localization of APE1, PARP-1 and OGG1, three important BER enzymes. Surprisingly, both mRNA and protein
levels for these enzymes are extremely reduced in XP-C deficient cells, contrasting to wild type, XP-A and CS-B
deficient cells. Interestingly, those differences are also seen for protein localization. Indeed, while PARP-1 keeps in
the nuclear compartment in XP-A and CS-B cells after H2O2 treatment, it is found both in nucleus and cytoplasm
in XP-C cells following treatment. Taken all together, our results reveal a role for XPC protein on the maintenance
of PARP-1 expression and its cellular localization, since the XPC deficiency promoted a reduced expression
level and a cytoplasmic localization of PARP-1, while they were not affected in XP-A and CS-B deficient cells.
Financial Support: CNPq, CAPES and Redoxoma.