Cryptic operon for b-glucoside metabolism in E.coli K12: genetic evidence for a regulatory protein (Articolo in rivista)

Type

• Prodotto della ricerca (Classe)
• Articolo in rivista (Classe)

Label

• Cryptic operon for b-glucoside metabolism in E.coli K12: genetic evidence for a regulatory protein (Articolo in rivista) (literal)

Anno

• 1981-01-01T00:00:00+01:00 (literal)

Alternative label

• Defez R., De Felice M. (1981)
  Cryptic operon for b-glucoside metabolism in E.coli K12: genetic evidence for a regulatory protein
  in Genetics (Austin Tex.)
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Defez R., De Felice M. (literal)

Pagina inizio

• 11 (literal)

Pagina fine

• 25 (literal)

Rivista

• Genetics (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

• 97 (literal)

Note

• PubMe (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• International Institute of Genetics and B:ophysics, C.N.R., Via Marconi IO, 80125 Naples, Italy (literal)

Titolo

• Cryptic operon for b-glucoside metabolism in E.coli K12: genetic evidence for a regulatory protein (literal)

Abstract

• Escherichia coli K12 does not metabolize beta-glucosides such as arbutin and salicin because of lack of expression of the bglBSRC operon, which contains structural genes for transport (bglC) and hydrolysis (bglB) of phospho-beta-glucosides. Mutants carrying lesions in the cis-acting regulatory site bglR metabolize beta-glucosides as a consequence of expression of this cryptic operon (Prasad and Schaefler 1974). We isolated mutations promoting beta-glucoside metabolism that were unlinked to bglR; some of these mutations were shown to be amber. All of them were mapped at 27 min on the E. coli K12 linkage map and appeared to define a single gene, for which we propose the designation bglY. Utilization of beta-glucosides in bglY mutants appeared to be a consequence of expression of the bglBSRC operon, since bglB bglR and bglB bglY double mutants had the same phenotype. All bglY mutations analyzed were recessive to the wild-type bglY+ allele. Phospho-beta-glucosidase B and beta-glucoside transport activities are inducible in bglY mutants, as they are in bglR mutants. Metabolism of beta-glucosides in both bglR and bglY mutants required cyclic AMP. We propose that bglY encodes a protein acting as a repressor of the bglBSRC operon, active in both the presence and absence of beta-glucosides, whose recognition site would be within the bglR locus. (literal)

Prodotto di

• Institute of genetics and biophysics \"Adriano Buzzati Traverso\" (IGB) (Istituto)
• Metodologie genomiche per le produzioni ecosostenibili e la tutela della salute (AG.P01.021.001) (Modulo)

Autore CNR

• ROBERTO DEFEZ (Unità di personale interno)

Incoming links:

Autore CNR di

• ROBERTO DEFEZ (Unità di personale interno)

Prodotto

• Institute of genetics and biophysics \"Adriano Buzzati Traverso\" (IGB) (Istituto)
• Metodologie genomiche per le produzioni ecosostenibili e la tutela della salute (AG.P01.021.001) (Modulo)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi

• Genetics (Rivista)