[en] The repair of the breaks in one of the strands in DNA double helixes is both efficient and rapid in living cells. The process involves the cleaning-up of the ends on either side of the break if necessary, the resynthesis of the missing part of the strand with the complementary strand as templete, and the sealing of the gap with a ligase. Double-strand breaks can be formed by the coincidence between random single-strand breaks in the complementary strands. Of greater importance are the double-strand breaks which resulted from a single primary event. The DNA obtained from bacteria, yeasts and mammalian cells which had been treated with X-ray will sediment faster on neutral density gradients if the cells have been incubated after the irradiation. The most solid evidence for the repair of double-strand breaks in bacteria comes from the experiments in which cells were irradiated, incubated to allow repair, then irradiated again. The sedimentation of such DNA from E. coli is greater than that from the cells which have not been incubated between two irradiations. The most convincing evidence for the repair of DNA double-strand breaks comes from the experiments in which cells were irradiated, incubated to produce repair, and then irradiated again. The repair of double-strand breaks is one of SOS functions. The cycloheximide at the concentration sufficient to block protein synthesis will also inhibit the repair of double-strand breaks in yeast cells. Although the events which may prevent cells from going through the normal replicative cycles are usually spoken as unrepaired double-strand breaks, it is possible that the lethal events may also be the misrepaired breaks, in which two ends are joined together incorrectly. (Yamashita, S.)