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. Author manuscript; available in PMC: 2013 May 3.
Published in final edited form as: Cancer Res. 2009 Jan 20;69(3):1143–1149. doi: 10.1158/0008-5472.CAN-08-3499

Figure 1.

Figure 1

LCL1261 cells are hPMS2 deficient and display a mutator phenotype. A, nuclear (nuc) and cytoplasmic (cyt) fractions were prepared from LCL721 and LCL1261 cells and analyzed for expression of MMR proteins (20 µg of total protein loaded) by Western blot analysis. The membrane was probed with hPMS2, hMLH1, hMSH2, hMSH6, and hMSH3. B, shuttle vectors containing [G/C]10 and [GT/CA]10 microsatellite alleles were introduced into LCL721 (hPMS2+) and LCL1261 (hPMS2−) cells. Individual plasmid-bearing clones were expanded from 24 to 35 cell generations. After extracting shuttle vector DNA, HSV-tk mutant frequencies were determined for each clone by selection in E. coli. The mutation rate was estimated by calculating the HSV-tk mutation frequency per cell generation. Mutational rate increase in the [G/C]10 and [GT/CA]10 vectors is shown as a proportion of the median mutation rate of LCL1261 clones versus LCL721.