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

Abstract:

: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.

authors

Morel P,Reverdy C,Michel B,Ehrlich SD,Cassuto E

doi

10.1073/pnas.95.17.10003

subject

Has Abstract

pub_date

1998-08-18 00:00:00

pages

10003-8

issue

17

eissn

0027-8424

issn

1091-6490

journal_volume

95

pub_type

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