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PARTICIPATION OF MOUSE DNA POLYMERASES IOTA, ETA, AND REV1 IN TRANSLESION SYNTHESIS OF CARCINOGEN INDUCED DNA ADDUCTS AND CARCINOGENESIS Chad Aaron Dumstorf March 21 , 2007 Recent advances in undE~rstanding the molecular mechanisms of mutagenesis indicate that most mutations are dependent on the activity of translesion synthesis DNA polymerases. The impact of reducing the level of these polymerases on mutageneslis and carcinogenesis in mouse models is poorly defined. Using knock out strategies we were able to remove polymerase eta (pol 11), and polymerase iota (pOll) and pol eta/pol iota from the mouse and lower REV1 in the mouse lung. This dissertation reports the changes in UVinduced carcinogenesis and mutagenesis that were observed. Mutagenesis data in pol iota. deficient cells clearly indicate pol iota as a mutagenic TLS polymerase in UV lesion bypass. Pol iota removal effectively lowered the mutational frequency in both pol eta null and wild-type backgrounds.

Participation of mouse DNA polymerases iota, eta, and rev1 in translesion synthesis of carcinogen induced DNA adducts and carcinogenesis.