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The Roles of Klenow Processing and Flap Processing Activities of DNA Polymerase I in Chromosome Instability in Escherichia coli K12 Strains
Yuki Nagataa, Kazumi Mashimoa, Masakado Kawataa, and Kazuo Yamamotoaa Department of Biomolecular Sciences, Graduate School of Life Sciences, Tohoku University, Sendai 980-8578, Japan
Corresponding author: Kazuo Yamamoto, Graduate School of Life Sciences, Tohoku University, Sendai 9808578, Japan., yamamot{at}mail.cc.tohoku.ac.jp (E-mail)
Communicating editor: R. MAURER
polA and polA107 mutant strains were compared. Five categories of mutations were found: (1) deletions, (2) minus frameshifts, (3) plus frameshifts, (4) duplications, and (5) other mutations. The
polA strain, which is deficient in both Klenow domain and 5'
3' exonuclease domain of DNA polymerase I, shows a marked increase in categories 14. The polA107 strain, which is deficient in the 5'
3' exonuclease domain but proficient in the Klenow domain, shows marked increases in categories 3 and 4 but not in 1 or 2. Previously, we reported that the polA1 strain, which is known to be deficient in the Klenow domain but proficient in the 5'
3' exonuclease domain, shows increases in categories 1 and 2 but not in 3 or 4. The 5'
3' exonuclease domain of DNA polymerase I is a homolog of the mammalian FEN1 and the yeast RAD27 flap nucleases. We therefore proposed the model that the Klenow domain can process deletion and minus frameshift mismatch in the nascent DNA and that flap nuclease can process plus frameshift and duplication mismatch in the nascent DNA.
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