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1
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A new look at adaptive mutations in bacteria.

100%
|
2000
|
vol. 47
|
issue 2
451-457
EN
This is a short survey of the adaptive mutation processes that arise in non- or slowly- dividing bacterial cells and includes: (i) bacterial models in which adaptive mutations are studied; (ii) the mutagenic lesions from which these mutations derive; (iii) the influence of DNA repair processes on the spectrum of adaptive mutations. It is proposed that in starved cells, likely as during the MFD phenomenon, lesions in tRNA suppressor genes are preferentially repaired and no suppressor tRNAs are formed as a result of adaptive mutations. Perhaps the most provocative proposal is (iv) a hypothesis that the majority of adaptive mutations are selected in a pre-apoptotic state where the cells are either mutated, selected, and survive, or they die.
2
100%
|
2001
|
vol. 48
|
issue 3
599-610
EN
The SOS system and SOS mutagenesis are frequently studied, or exploited to obtain an increase in mutagenicity of bacteria. Here a short survey is made of the phenomenon of SOS response with special attention to latest and less discussed data, especially the induction of the SOS system in response to cell starvation or mutation of certain genes and the role of inducible DNA polymerases.
3
Content available remote

Mutator specificity of Escherichia coli alkB117 allele

51%
|
2006
|
vol. 53
|
issue 2
425-428
EN
The Escherichia coli AlkB protein encoded by alkB gene was recently found to repair cytotoxic DNA lesions 1-methyladenine (1-meA) and 3-methylcytosine (3-meC) by using a novel iron-catalysed oxidative demethylation mechanism that protects the cell from the toxic effects of methylating agents. Mutation in alkB results in increased sensitivity to MMS and elevated level of MMS-induced mutations. The aim of this study was to analyse the mutational specificity of alkB117 in a system developed by J.H. Miller involving two sets of E. coli lacZ mutants, CC101-106 allowing the identification of base pair substitutions, and CC107-CC111 indicating frameshift mutations. Of the six possible base substitutions, the presence of alkB117 allele led to an increased level of GC→AT transitions and GC→TA and AT→TA transversions. After MMS treatment the level of GC→AT transitions increased the most, 22-fold. Among frameshift mutations, the most numerous were -2CG, -1G, and -1A deletions and +1G insertion. MMS treatment appreciably increased all of the above types of frameshifts, with additional appearance of the +1A insertion.
8
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Is the tRNA ochre suppressor supX derived from gltT?

32%
9
Content available remote

Some problems of mutagenssis induced by base analogues

32%
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