Endonuclease G: a role for the enzyme in recombination and cellular proliferation.
Our earlier studies had suggested that endonuclease G (EndoG), a member of the evolutionarily conserved DNA/RNA nonspecific betabetaalpha-Me-finger nuclease family, functioned in the a sequence-mediated segment inversion observed during herpes simplex virus 1 replication. To test this hypothesis, we used RNA interference to reduce the level of EndoG in mammalian cells in culture. Reduction of EndoG produced a small but statistically significant decrease in a sequence-mediated recombination, suggesting that EndoG does play a role in this process. We also observed that reduction in the level of EndoG resulted in a deficiency in cell proliferation. Cells with a reduced level of EndoG also showed changes in cell distribution in the cell cycle, producing a pattern characteristic of cells that have been arrested in the G(2) phase. These findings suggest that EndoG is required for normal cellular proliferation.
Huang
Ke-Jung
KJ
Departments of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305, USA.
Ku
Chia-Chi
CC
Lehman
I Robert
IR
D000818:Animals; D001483:Base Sequence; D002453:Cell Cycle / Q000502:physiology; D049109:Cell Proliferation; D002470:Cell Survival; D002522:Chlorocebus aethiops; D004706:Endodeoxyribonucleases / Q000235:genetics / Q000378:metabolism*; D018259:Herpesvirus 1, Human / Q000235:genetics; D006801:Humans; D008969:Molecular Sequence Data; D034622:RNA Interference; D011995:Recombination, Genetic; D014709:Vero Cells
D004706:Endodeoxyribonucleases; C052391:endonuclease G