Abstract
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 subsequently 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 previous study using the fission yeast Schizosaccharomyces pombe as a model organism has revealed that X-irradiation elevates recombination frequency for about 10 cellular generations after recovery from the cell cycle arrest, and that delayed activation of a recombination repair protein Rad22 is also induced by X-ray in the dividing cells for a period similar to that of the delayed recombination. However, the regulation mechanism of delayed activation of Rad22 is remained to be elucidated.
We have been challenging to search regulator of Rad22 activity during the delayed recombination. We characterized at least 9 proteins as the components of the Rad22 complex which include single stranded DNA binding proteins, heat shock proteins, repair proteins and other proteins thought to be related to chromatin and/or genomic maintenance. In such a criterion that the change of expression levels affects recombination frequency, we screened possible regulators among the components of Rad22 complex. They might be important factor for the delayed mutation.
