. Author manuscript; available in PMC: 2009 Oct 1.

Published in final edited form as: DNA Repair (Amst). 2008 Aug 3;7(10):1636–1646. doi: 10.1016/j.dnarep.2008.06.008

Table 4.

TLS across a site-specific TT 6-4 PP in polη-proficient and polη-deficient human cells

Cell type		Transformants		Plasmid repair, %	TLS, %
Cell type		Kan^R	Cm^R	Plasmid repair, %	TLS, %
Primary fibroblasts	POLH^+/+	323	2064	14±3	13±3
Primary fibroblasts	POLH^−/− (XPV)	274	2207	12±2	11±2
SV-40 transformed fibroblasts	POLH^+/+	154	332	41±4	40±4
SV-40 transformed fibroblasts	POLH^−/− (XPV)	342	1022	29±2	28±2
Burkitt's lymphoma cells	POLH^+/+	88	566	15±2	14±1
Burkitt's lymphoma cells	POLH^−/−	68	790	8±1	7±1

The experiments were performed as described in the legend to Table 1, except that the gap-lesion plasmid was GP-TT-6-4-PP (kanR). The extent of plasmid repair was calculated by the kan^R/cm^R ratio, and the extent of TLS was obtained by calculating this value by the percentage of TLS events out of all repair events, as determined by DNA sequence analysis, and shown in Table 5 and Table 6. The colony counts are of a representative experiment. The efficiencies of plasmid repair and TLS were obtained by averaging the results of at least three experiments.