Student: Stephen Mastrinao
Mentor: Professor Suzanne Deschenes
Major: Biology

Spontaneous mutations that arise from replication errors and endogenous DNA damage usually occur only at low frequencies because of the action of different DNA repair pathways.  Sodium nitrite (SN) is known to be harmful to organisms because it causes base substitutions by deaminating adenine to form hypoxanthine, guanine to form xanthine, and cytosine to form uracil.  The deaminations caused by SN may prevent bases from pairing properly with their complementary bases.  In E. coli two repair mechanisms that are known to correct DNA damage caused by NA are base excision repair and endonuclease V (EndoV).  However, we hypothesize that mismatch repair (MMR), which has the capacity to recognize mispaired bases, also plays a role in preventing SN mutagenesis.  In previous work we constructed MMR deficient versions of E. coli lacZ reversion strains, and performed preliminary SN mutagenesis studies under micro-aerobic conditions.  Here, we provide additional SN mutagenesis data on the MMR deficient strains, and describe the construction of EndoV-deficient versions of the E. coli lacZ reversion strains.  Our results suggest that MMR may play a significant role in preventing SN-induced mutations such as A:T?G:C, +1A, and -1A.  Furthermore, we successfully optimized an EndoV transduction protocol, and identified CC106 EndoV- deficient strains through PCR genotyping.  In future work, SN mutagenesis studies in MMR deficient strains will be replicated and double mutant strains lacking EndoV and MMR will be created for additional mutagenesis studies.

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