Host: The Japan Radiation Research Society, Chairman of the 52nd Annual Meeting, Toshiteru Okubo (Radiation Effects Research Foundation)
It is known that genomic lesion introduced by ionizing radiations continuously activates cellular responses against DNA damage even after completion of damage repair of the initial dose, and induces genomic instability or upregulation of mutation rate for a period. This phenomenon is called delayed mutation which is thought as a result of epigenetic damage memory and mutagenic activity at the downstream of the memory.
Our study using the fission yeast Schizosaccharomyces pombe as a model organism has revealed that (i) X-irradiation elevates recombination frequency for about 10 cellular generations after recovery from the cell cycle arrest, (ii) the delayed recombination is possible to occur in trans, or would have a weak relation to the position of the initial damage site and the production of reactive oxygen species induced by the damage, (iii) delayed activation of a recombination repair protein Rad22 is also induced by X-ray in the dividing cells, and (iv) the activation of Rad22 continues for a period similar to that of the delayed recombination. These results suggest that Rad22 has a critical role in the delayed recombination. However, the regulation mechanism of delayed activation of Rad22 is remained to be elucidated.
Now we are challenging to screen regulator of Rad22 with mass spectrometric analysis combined with pull-down assay using Rad22 as bait. We will present a result of screening of the regulator to date with a brief summary of the studies on the delayed mutation and the damage memory.
