Logarithmically growing bacteria differ from stationary phase bacteria with respect to the number of genome copies present in the cell, and this has implications for the capability to carry out an important DNA repair process. During logarithmic growth, two or more copies of any particular region of the chromosome may be present in a bacterial cell, as cell division is not precisely matched with chromosome replication. The process of homologous recombinational repair (HRR) is a key DNA repair process that is especially effective for repairing double-strand damages, such as double-strand breaks. This process depends on a second homologous chromosome in addition to the damaged chromosome. During logarithmic growth, a DNA damage in one chromosome may be repaired by HRR using sequence information from the other homologous chromosome. Once cells approach stationary phase, however, they typically have just one copy of the chromosome, and HRR requires input of homologous template from outside the cell by transformation. 
The study of transformation dates to the late 1920s, when an English physician, F. Griffith, discovered that pneumococcal cells ( Streptococcus pneumoniae ) could convert from a harmless form to a disease-causing type. He noticed that pneumococci may or may not have a capsular covering. Those cells with a capsule (forming smooth colonies) caused disease in mice; those lacking a capsule (and forming rough-surfaced colonies) were harmless. A mixture of living, nonencapsulated cells and heat-killed, capsulated cells, when inoculated into mice, caused disease. Living, encapsulated cells (pathogenic) were created by a “transforming principle” liberated from the dead cells to the living cells. The transformation was heritable. In 1943 a group of investigators at the Rockefeller Institute, New York City , identified that “transforming principle” as DNA.