ArticleMolecular genetics and genomics : MGG2003
Mutations arise independently of transcription in non-dividing bacteria.
Article in Molecular genetics and genomics : MGG, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Stress-Induced Mutagenesis.EcoSal Plus · 2012Article
- Stress-induced mutagenesis in bacteria.Critical reviews in biochemistry and molecular biologyReview
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been proposed that transcription introduces a bias into the random process of mutation. Although this hypothesis is supported by experimental data for mutations arising during active bacterial growth, the role of transcription in mutagenesis in non-dividing bacteria is entirely hypothetical. In the present study, we tested the hypothesis of a possible role of transcription in a non-dividing E. coli K12 strain. In this strain (BD010), a mutated trpB allele (trpB9578), placed under stringent transcriptional control, was tested for the appearance of prototrophic revertants on synthetic medium lacking tryptophan. The number of phenotypic revertants which appeared in the absence of trp transcription was compared to that observed when the mutated gene was continuously transcribed. Our results showed that transcription of trpB is not mutagenic under conditions of tryptophan starvation, and that the frequency of TrpB+ reversion is solely a function of the duration of starvation.
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