Use of data from bacteria to interpret data on DNA damage processing in mammalian cells

Abstract

The most important reason for determining the changes in base sequence in the processing of DNA damage is to determine mechanisms. Currently, much more is known about these mechanisms in prokaryotes, partly because the experiments are easier and quicker to do in bacteria, and partly because of the wealth of well characterized bacterial mutants deficient in various DNA repair pathways. This paper summarizes some information on the mechanisms in bacteria that are involved in the induction by various agents of base change mutations, 1- and 2-base deletions or additions that cause frameshifts, and more complicated insertions and deletions that involve up to tens of base pairs. For gross DNA rearrangements such as large deletions involving hundreds or thousands of base pairs, there is actually more information available in mammalian cells than in bacterial cells. It is suggested that deletions of several kilobases or more in bacteria are not easy to detect because they have a high probability of deleting both the gene under study and an adjacent essential gene, forming a nonviable cell. In mammalian cells, the large size (30–40-kb pairs) of the average gene, including both introns and exons, means that a large deletion is more likely to be confined to a single gene and less likely to lead to a nonviable cell.