Abstract
1Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America, 2University ofPittsburgh Cancer Institute, Hillman Cancer Center, Pittsburgh, Pennsylvania, United States of America, 3Department of Human Genetics, University of PittsburghGraduate School of Public Health, Pittsburgh, Pennsylvania, United States of America
Highlights
In this issue of PLOS Genetics, Sweasy and colleagues conducted a detailed analysis of the POLB germline–coding SNP rs3136797 [22]
To determine whether the P242R mutation affected genome stability in human or mouse cells, the wild-type (WT) or P242R protein was produced in human normal mammary epithelial cells (MCF10A) and in mouse embryonic fibroblasts (MEFs)
The cells were treated with methyl methanesulfonate (MMS) to induce DNA damage repaired by polymerase ß (Polß) [5]
Summary
In this issue of PLOS Genetics, Sweasy and colleagues conducted a detailed analysis of the POLB germline–coding SNP rs3136797 [22]. Cancerspecific mutations in Polß (e.g., Y265C) induced an increase in mutant frequency [23,24] that could explain the increase in chromosome alterations seen with P242R. Cells producing the P242R protein were found to have the same mutant frequency as those expressing WT Polß.
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