The base analogue 6-N-hydroxylaminopurine (HAP) is a potent mutagen in a variety of prokaryotic and eukaryotic organisms. Mutations in the yeast ham1 gene render the cells hypersensitive to the mutagenic effect of HAP. We have found that this gene has homologues in a variety of organisms from bacteria to man. We have overexpressed yeast Ham1p in E. coli. We demonstrate that under conditions when this protein constitutes approximately 30% of cellular protein, the host strain is protected both from toxic and mutapgenic effects of HAP. This result indicates that sole Ham1p activity might be sufficient for destruction of HAP or its metabolites in bacterial cells.
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