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Vol 50(2016) N 2 p. 252-261; DOI 10.1134/S0026893316020175 Full Text

V. Misic1*, M. El-Mogy1,2, S. Geng1,3, Y. Haj-Ahmad1

Effect of endonuclease G depletion on plasmid DNA uptake and levels of homologous recombination in hela cells

1Department of Biological Sciences, Brock University, St. Catharines, ON, Canada
2Molecular Biology Department, National Research Centre, Dokki, Giza, Egypt
3Montreal Neurological Institute, Montreal, Quebec, Canada

*vanjamisic.bu@gmail.com
Received - 2015-05-02; Accepted - 2015-06-24

Endonuclease G (EndoG) is a mitochondrial apoptosis regulator that also has roles outside of programmed cell death. It has been implicated as a defence DNase involved in the degradation of exogenous DNA after transfection of mammalian cells and in homologous recombination of viral and endogenous DNA. In this study, we looked at the effect of EndoG depletion on plasmid DNA uptake and the levels of homologous recombination in HeLa cells. We show that the proposed defence role of EndoG against uptake of non-viral DNA vectors does not extend to the cervical carcinoma HeLa cells, as targeting of EndoG expression by RNA interference failed to increase intracellular plasmid DNA levels. However, reducing EndoG levels in HeLa cells resulted in a statistically significant reduction of homologous recombination between two plasmid DNA substrates. These findings suggest that non-viral DNA vectors are also substrates for EndoG in its role in homologous recombination.

endonuclease G, homologous recombination, DNase, exogenous DNA, HeLa cells



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