Abstract
Living in an oxygen-rich environment is dangerous for a cell. Reactive oxygen species can damage DNA, RNA, protein and lipids. The MutT protein in Escherichia coli removes 8-oxo-deoxyguanosine triphosphate (8-oxo-dGTP) and 8-oxo-guanosine triphosphate (8-oxo-GTP) from the nucleotide pools precluding incorporation into DNA and RNA. While 8-oxo-dGTP incorporation into DNA is mutagenic, it is not clear if 8-oxo-GTP incorporation into RNA can have phenotypic consequences for the cell. We use a bistable epigenetic switch sensitive to transcription errors in the Escherichia coli lacI transcript to monitor transient RNA errors. We do not observe any increase in epigenetic switching in mutT cells. We revisit the original observation of partial phenotypic suppression of a lacZamber allele in a mutT background that was attributed to RNA errors. We find that Lac+ revertants can completely account for the increase in β-galactosidase levels in mutT lacZamber cultures, without invoking participation of transient transcription errors. Moreover, we observe a fluctuation type of distribution of β-galactosidase appearance in a growing culture, consistent with Lac+ DNA revertant events. We conclude that the absence of MutT produces a DNA mutator but does not equally create an RNA mutator.
Highlights
Errors in information transfer from DNA to RNA to protein are inevitable
It is clear that incorporation of 8-oxo-dGTP into DNA can have mutagenic consequences for the cell, with heritable phenotypic consequences, it remains unknown if incorporation of 8-oxo-GTP into RNA can have heritable phenotypic consequences for the cell (26)
It was suggested that the lacI gene has an inefficient promoter and that only one or two mRNA molecules are synthesized per lacI gene per generation (28)
Summary
Errors in information transfer from DNA to RNA to protein are inevitable. Transcription errors occur at a rate of ∼10−5 per residue in Escherichia coli (1,2), over 10 000×higher than errors in DNA synthesis.
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