PMID:1921981: Difference between revisions

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<span style = 'font-size: large'> '''Volkert, MR and Hajec, LI'''  (1991) Molecular analysis of the aidD6::Mu d1 (bla lac) fusion mutation of Escherichia coli K12.''Mol. Gen. Genet.'' '''229''':319-23</span>
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!align=left  |Citation
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'''No author listed'''  (1991) Molecular analysis of the aidD6::Mu d1 (bla lac) fusion mutation of Escherichia coli K12. ''Mol. Gen. Genet.'' '''229''':319-23
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!align=left  |Abstract
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In this report we present genetic and biochemical evidence indicating that the aidD6::Mu d1 (bla lac) fusion is an insertion of Mu d1 (bla lac) into the alkB coding sequence. We describe the phenotypic effects resulting from this mutation and compare them with the effects of alkB22, alkA and ada mutations. We also constructed an alkA alkB double mutant and compared its phenotype with that of the single mutant strains. The observation that the methyl methanesulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) resistance of the double mutant is approximately at the level predicted from the additive sensitivity of each of the single mutants suggests that these two gene products act in different pathways of DNA repair.
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!align=left  |Links
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1921981 PubMed]


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|{{TableHeadingColor}} |'''Abstract''' || In this report we present genetic and biochemical evidence indicating that the aidD6::Mu d1 (bla lac) fusion is an insertion of Mu d1 (bla lac) into the alkB coding sequence. We describe the phenotypic effects resulting from this mutation and compare them with the effects of alkB22, alkA and ada mutations. We also constructed an alkA alkB double mutant and compared its phenotype with that of the single mutant strains. The observation that the methyl methanesulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) resistance of the double mutant is approximately at the level predicted from the additive sensitivity of each of the single mutants suggests that these two gene products act in different pathways of DNA repair.
!align=left  |Keywords
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Alkylation; Escherichia coli/drug effects; Escherichia coli/genetics; Genetic Complementation Test; Methyl Methanesulfonate/toxicity; Methylnitronitrosoguanidine/toxicity; Mutation; Phenotype; Restriction Mapping; Species Specificity
|{{TableHeadingColor}} nowrap |'''Links''' ||  [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1921981 PubMed]
 
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==Significance {{HelpIcon|Help:Literature}} ==
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}
{{LitSignificance}}

Revision as of 19:06, 1 September 2013

Citation

No author listed (1991) Molecular analysis of the aidD6::Mu d1 (bla lac) fusion mutation of Escherichia coli K12. Mol. Gen. Genet. 229:319-23

Abstract

In this report we present genetic and biochemical evidence indicating that the aidD6::Mu d1 (bla lac) fusion is an insertion of Mu d1 (bla lac) into the alkB coding sequence. We describe the phenotypic effects resulting from this mutation and compare them with the effects of alkB22, alkA and ada mutations. We also constructed an alkA alkB double mutant and compared its phenotype with that of the single mutant strains. The observation that the methyl methanesulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) resistance of the double mutant is approximately at the level predicted from the additive sensitivity of each of the single mutants suggests that these two gene products act in different pathways of DNA repair.

Links

PubMed

Keywords

Alkylation; Escherichia coli/drug effects; Escherichia coli/genetics; Genetic Complementation Test; Methyl Methanesulfonate/toxicity; Methylnitronitrosoguanidine/toxicity; Mutation; Phenotype; Restriction Mapping; Species Specificity

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