A class of gyrB mutants, substantially unaffected in DNA topology, suppresses the Escherichia coli K12 ftsZ84 mutation. (Articolo in rivista)

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  • A class of gyrB mutants, substantially unaffected in DNA topology, suppresses the Escherichia coli K12 ftsZ84 mutation. (Articolo in rivista) (literal)
Anno
  • 1991-01-01T00:00:00+01:00 (literal)
Alternative label
  • Ruberti, I., Crescenzi, F., Paolozzi, L., Ghelardini, P. (1991)
    A class of gyrB mutants, substantially unaffected in DNA topology, suppresses the Escherichia coli K12 ftsZ84 mutation.
    in Molecular microbiology (Online); BLACKWELL SCIENCE LTD, Oxford (Regno Unito)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Ruberti, I., Crescenzi, F., Paolozzi, L., Ghelardini, P. (literal)
Pagina inizio
  • 1065 (literal)
Pagina fine
  • 1072 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 5 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Centro di studio sugli Acidi Nucleici, CNR (literal)
Titolo
  • A class of gyrB mutants, substantially unaffected in DNA topology, suppresses the Escherichia coli K12 ftsZ84 mutation. (literal)
Abstract
  • Previous work in our laboratory suggested that DNA topology could be implicated in the regulation of the division gene ftsZ. To settle this question, we have selected and characterized mutants in the gyrB gene able to phenotypically suppress the defects of the ftsZ84 mutation. No strict correlation was found between the degree of plasmid DNA relaxation and the level of suppression of the thermosensitivity of the ftsZ84 strain. Interestingly, the class of mutants that shows maximal suppression is substantially unaffected in DNA topology. In addition, the amount of ftsZ-specific mRNA in this class of mutants is comparable to that present in the ftsZ84 strain. These results hint that the ability of these gyrB mutants to correct the effects of the ftsZ84 mutation is largely unrelated to the function of the GyrB (as a part of DNA gyrase) in the control of DNA superhelicity and suggest hitherto unsuspected interaction between the ftsZ and gyrB gene products. (literal)
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