THE NATURE OF THE SOS-INDUCING LESIONS CAUSED BY UV LIGHT IN E. COLI CELLS DEFICIENT IN UMU C GENE PRODUCT

摘要

A major repair mechanism in Exoli cells is nucleotide excision repair. This process is initiated by the Uvr ABC nuclease which provides damage recognition and incision. The rate of incision is limited by the number of UvrC molecules per cell (approximately 20). Products of polA and uvrD genes are required to complete repair, release Uvr complex from DNA and thus stimulate turnover of enzymes [1, 2].