Search PubMed⌕ Search

Biomedical subjects

S Adhya

Publications and source records attributed to S Adhya.

85 records · Page 5Linked to original sources
PubMed1974

Release of polarity in Escherichia coli by gene N of phage lambda: termination and antitermination of transcription.

The induction of lambda prophage provokes the constitutive expression of the adjacent gal operon in E. coli. This "escape synthesis" can result from transcription that initiates at a phage promoter and extends into the gal operon. The effect requires the product of the lambda gene N. N-mediated transcription not only fails to terminate at the prophage-bacterial junction and at the ends of bacterial operons, but ignores termination signals caused by polar insertions or ochre mutations within gal. Suppression of polarity by N-function is a cis-effect; only transcription initiated at the phage promoter is influenced. We propose that the transcription complex is influenced by N-product to become termination-resistant at a site in the phage genome (juggernaut model). This site appears to be at or near the phage promoter.

Chromosome Mapping↗
PubMed1973

In vitro repression of the transcription of gas operon by purified gal repressor.

We have studied the in vitro repression of gal mRNA synthesis by the gal repressor from Escherichia coli. By use of a four-step purification procedure involving chromatography on phosphocellulose, DEAE-cellulose, and an affinity resin, the gal repressor has been purified about 1600-fold from a crude cell extract. The purification was aided by use of a cell extract made after prophage induction of cells lysogenic for bacteriophage lambda that carries the gal repressor gene (galR). The highly purified gal repressor is an effective and specific repressor of in vitro synthesis of gal mRNA with lambda gal DNA as template. Both D-fucose and D-galactose overcome the action of gal repressor; the half-maximal concentrations of D-fucose and D-galactose for overcoming the action of repressor are 1 mM and 0.5 mM, respectively. The repressor fails to repress gal-specific transcription when the gal DNA contains a cis-dominant operator constitutive (O(c)) mutation. We conclude that the gal repressor recognizes the gal operator site and acts by preventing gal transcription.

Ammonium Sulfate↗
PubMed1971

Phosphoglucomutase mutants of Escherichia coli K-12.

Bacteria with strongly depressed phosphoglucomutase (EC 2.7.5.1) activity are found among the mutants of Escherichia coli which, when grown on maltose, accumulate sufficient amylose to be detectable by iodine staining. These pgm mutants grow poorly on galactose but also accumulate amylose on this carbon source. Growth on lactose does not produce high amylose but, instead, results in the induction of the enzymes of maltose metabolism, presumably by accumulation of maltose. These facts suggest that the catabolism of glucose-1-phosphate is strongly depressed in pgm mutants, although not completely abolished. Anabolism of glucose-1-phosphate is also strongly depressed, since amino acid- or glucose-grown pgm mutants are sensitive to phage C21, indicating a deficiency in the biosynthesis of uridine diphosphoglucose or uridine diphosphogalactose, or both. All pgm mutations isolated map at about 16 min on the genetic map, between purE and the gal operon.

Bacteriological Techniques↗
PubMed1966

Glucose effect and the galactose enzymes of Escherichia coli: correlation between glucose inhibition of induction and inducer transport.

Adhya, Sankar (University of Wisconsin, Madison), and Harrison Echols. Glucose effect and the galactose enzymes of Escherichia coli: correlation between glucose inhibition of induction and inducer transport. J. Bacteriol. 92:601-608. 1966.-The inhibitory effect of glucose on the induction of the enzymes required for galactose utilization ("glucose effect") was studied in Escherichia coli. Experiments on the uptake into the cell of labeled inducers (d-galactose-C(14) and d-fucose-H(3)) pointed to inhibition at the level of inducer transport as the possible primary mechanism of the glucose effect in the case of the gal enzymes. This interpretation was supported by the finding that a mutant constitutive for the lac enzymes was resistant to glucose inhibition of galactose induction of the gal enzymes; the mutant had acquired a glucose-resistant alternative transport mechanism for galactose via the constitutively synthesized galactoside permease. Further support for the transport inhibition model was provided by the finding that glucose did not substantially inhibit induction of the gal enzymes when glucose and galactose were produced intracellularly by beta-galactosidase hydrolysis of lactose, even if excess glucose was added. The inducer uptake experiments also showed that d-galactose and d-fucose probably enter the cell via different transport systems, although uptake of both compounds was inhibited by glucose.

Carbon Isotopes↗