Mechanism of spontaneous loss of heat-stable toxin (STa) production in enterotoxigenic Escherichia coli.Five strains of enterotoxigenic Escherichiu coli (ETEC) showing spontaneous loss of heat-stable enterotoxin (STa) production were studied to elucidate the underlying genetic mechanisms. Southern blot analysis revealed that loss of STa production. and the corresponding lack of hybridization with the STa gene probes, were associated with deletions of DNA fragments harboring the relevant toxin genes rather than with loss of plasmids.
SUMMARY3-Methyladenine-DNA glycosylase activities have been identified in all eukaryotic cell systems studied. Some of the results from these studies are reviewed here. The enzymes possess molecular weights between 24X103 and 34X103, they have a broad pH optimum at approximately pH 8, require double-stranded DN A and act in the absence of any cofactors. The enzyme can excise several different methylated bases from D N A such as 3-methyladenine, 7-methylguanine and 3-methylguanine.The specific activity of this D N A glycosylase in mouse L-cells was found to be a function of the proliferative state of the cell. In vitro quantification of this DN A repair activity in synchronized mouse L-cells suggests that it is regulated within a defined temporal sequence prior to the onset of D N A replication. Using D N A fragments of defined sequences it was observed that the efficiency of removal of the methylated bases is sequence-dependent.
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