Investigations to the DNA resection regulation of ion-induced DSBs
in G1 cells and the resection limitations of the cells in quiescent state
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Complex DNA double-strand breaks (DSB) are the most severe DNA damage in that they represent an enormous challenge for the cell to repair faithfully as well as repairing at all. Two main repair pathways are known to repair DSBs: classical non-homologous end joining (c-NHEJ) and homologous recombination (HR). c-NHEJ is available in all cell cycle phases whereas the HR pathway functions only in S/G2 when the sister chromatid is available as a template. In addition, a further repair pathway is available to the cells - alternative non-homologous end joining (alt- NHEJ), which can operate on resect...
Complex DNA double-strand breaks (DSB) are the most severe DNA damage in that they represent an enormous challenge for the cell to repair faithfully as well as repairing at all. Two main repair pathways are known to repair DSBs: classical non-homologous end joining (c-NHEJ) and homologous recombination (HR). c-NHEJ is available in all cell cycle phases whereas the HR pathway functions only in S/G2 when the sister chromatid is available as a template. In addition, a further repair pathway is available to the cells - alternative non-homologous end joining (alt- NHEJ), which can operate on resected DNA break ends. DNA resection is an important step in the cell's decision as to which DSB repair pathway to choose. DNA resection takes place not only in S/G2 cells but also in G1 cells following complex DNA damage induced by heavy ion radiation. The goal of this work is to elucidate the mechanism of resection regulation in G1 cells after heavy ion irradiation. It specifically focuses on the role of the resection regulatory factors RIF1 and BRCA1. A useful model to study the mechanism of resection limitation are cells in quiescent state, G0 cells.
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