The role of SOS and flap processing in microsatellite instability in Escherichia coli.

نویسندگان

  • P Morel
  • C Reverdy
  • B Michel
  • S D Ehrlich
  • E Cassuto
چکیده

Mutations affecting mismatch repair result in elevated frequencies of microsatellite length alteration in prokaryotes and eukaryotes. However, the finding that microsatellite instability is found often in cells with a functional mismatch repair system prompted a search for other factors of tract alteration. In the present report, we show that, in Escherichia coli, poly(AC/TG) tracts are destabilized by mutations that induce SOS. These observations may have implications for eukaryotic cells because recent results suggest the existence of a mammalian SOS response analogous to that in prokaryotes. In addition, a defect in the 5'-3' exonuclease domain of DNA polymerase I, homologous to the mammalian FEN1 and the yeast RAD27 nucleases, leads to a marked increase in repeat expansions characteristic of several genetic disorders. Finally, we found that the combination of a proofreading defect with mismatch repair deficiency results in extreme microsatellite instability.

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عنوان ژورنال:
  • Proceedings of the National Academy of Sciences of the United States of America

دوره 95 17  شماره 

صفحات  -

تاریخ انتشار 1998