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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As an effort to elucidate the control of quality and quantity of the DNA-dependent RNA polymerase in Escherichia coli, the rate of synthesis of the individual subunits was determined during shift-up and -down of nutrients. When the strain B/r grown in a succinate medium was imposed to a shift-up by adding a mixture of glucose and amino acids, rapid rise was observed of the differential rates of the synthesis of alpha, beta and beta' subunits, the constituents of core enzyme, leading to the increase of core polymerase concentration. The differential rates decreased thereafter to the level characteristic of the post-shift rate of cell growth. Compared to the strain B/r, the adaptation was slow in the strain K12 W3350. On the other hand, upon transfer of the strain B/r from a glucose-amino acids medium to a glucose medium lacking amino acids, the differential rate of core polymerase synthesis decreased rapidly and then regained the rate characteristic of the new growth rate. Similar control was also observed on the rate of ribosomal protein synthesis suggesting the coordinate expression of genes for the core polymerase subunits and ribosomal proteins. Thus, the intracellular concentration of RNA polymerase as well as of ribosomes might be one of the most important factors that affect the rate of bacterial growth. The rate of alpha subunit synthesis, however, exhibited little change during the shift-up but a considerable decrease was observed during the shift-down.
Mol Gen Genet 1975 Dec 23
PMID:Biosynthesis of RNA polymerase in Escherichia coli. II. control of RNA polymerase synthesis during nutritional shift up and down. 76 37

An inorganic phosphate transport mutant has been isolated as a sn-glycerol-3-phosphate auxotroph and characterized genetically. Two lesions are responsible for the transport defect. One lesion, pst, is located at minute 74 of the E. coli genetic map while the other lesion, pit, is located at minute 68. All "K10" strains that were examined carry the pit lesion. Evidence is presented that the glycerol phosphate and hexose phosphate transport systems are not important inorganic phophate transport systems. The mapping data indicate that the genetic distance between malA and xyl is greater than that now allowed.
Mol Gen Genet 1975 Dec 30
PMID:A mutant of Escherichia coli auxotrophic for organic phosphates: evidence for two defects in inorganic phosphate transport. 76 45

The isolation and properties of a new radiation sensitive mutant of Escherichia coli K-12 are described which shows a correlation between radiation sensitivity and replication of irradiated DNA. The mutation, called rer, is located between arg B and pur D loci. The mutant, when grown in tryptone broth after irradiation, is sensitive to UV and lambda-rays and incorporates little or no 3H-thymidine but in minimal glucose-salts medium both the radiation sensitivity and incorporation of 3H-thymidine remain identical to that of the parent strain. Studies with a temperature sensitive double mutant rer dnaC show that 1 hr incubation of irradiated cells at 42 degrees C before their transfer to 30 degrees C results in higher survival as compared to their incubation at 30 degrees C only. It is suggested that rer controls the replication of irradiated DNA and thus regulates the coordination between replication and repair of DNA.
Mol Gen Genet 1976 Feb 02
PMID:Radiation sensitivity of a mutant of Escherichia coli K-12 associated with DNA replication: evidence for a new repair function. 76 65

Kinetics was studied of DNA degradation, processing and synthesis in the course of post-radiation incubation (irradiation dose 0-2000 erg/mm2). It has been shown that contrary to the endonuclease splitting of DNA strands, DNA degradation requires energy. DNA degradation is not enhanced upon an increase of the irradiation up to 400 erg/mm2 and more and at the incubation duration exceeding 120 min. The degradation involves not more than 40% of the total DNA quantity. It takes place in the absence of resynthesis registered by the incorporation of [3h] thymidine and 32P and dephinylamine reaction. The number of single-strand breaks in DNA (per one E. coli chromosome strans) reaches a maximum value after 120-180 min. of incubation. This maximal value is linearily increased upon an increase of the irradiation dose from 0 to 1200 erg/mm2 and does not change when the dose increases further. The number of single-strand breaks does not exceed 35-50, this value being dependent on the presence of glucose. On the basis of the data obtained a suggestion is put forward that in the course of the reparative degradation of DNA, prolonged (10(4)-10(5) nucleotides) single-stranded regions are formed. Possible role of these 'nicks" in the appearance of mutations is discussed.
Mol Biol (Mosk)
PMID:[Structure of the DNA molecule in the course of reparation process after ultraviolet irradiation of E. coli cells]. 76 45

Alterations in the physical characteristics of mitochondrial DNA accompanied increased spontaneous mutability to cytoplasmic respiratory-deficiency in yeast. Two systems were used to modify mutation rates, one physiological, the other genetic. Cells in log phase were shown to be more mutable than cells in stationary phase, and glucose-repressed cells were shown to be more mutable than unrepressed cells. A nuclear gene which acts as a mitochondrial mutator was found to increase spontaneous mutation rate by a factor of ten. An increase in endogenous formation of G+G-rich fragments of mt-DNA accompanied a physiological state conducive to higher mutability, and it is proposed that increased in vivo digestion of A+T-rich regions is involved in these alterations. Greater nuclease(s) activity accompanied the presence of the mutator gene, and it is proposed that this gene is concerned with the regulation of nuclease activity or with repair mechanisms.
Mol Gen Genet 1976 Mar 22
PMID:Alterations in mitochondrial DNA of yeast which accompany genetically and environmentally controlled changes in rho- mutability. 77 86

A mutant strain (2-20) isolated by growth on medium containing oligomycin and cycloheximide was also found to be cross resistant to antimyicn, cerulenin, chloramphenicol, tetracycline, triethyltin and triphenylmethylphosphonium bromide, but collaterally sensitive to dequalinium chloride, gentamycin, neomycin, paromomycin and thiolutin. Growth of 2-20, compared to the parental strain and 2 complete revertants, under a variety of environmental conditions revealed that strain 2-20 had an enhanced sensitivity to increased osmolality, elevated pH, and high temperature; in addition, strain 2-20 was unable to polymerize aminoimidazole ribotide at 37 degrees C as shown by the failure to develop a red colony in the presence of ade 2. Four complex solid media (glucose--KCI, galactose, ethanol, ethanol--KCI, Table 1) unable to sustain the growth of strain 2-20 were arbitrarily chosen to monitor cellular growth under different physiological conditions. Tetrad analysis indicated that the complex phenotype (cross resistance, collateral sensitivity, inablity to polymerize aminoimidazole ribotide, absence of growth under adverse physiological conditions) was inherited by an allele of a locus previously shown to result in a permeability barrier of the plasma membrane to chloramphenicol. 582 of 640 subclones used to isolate revertants of 2-20, under four different physiological conditions, were observed to produce a complete revertant of the complex phenotype. It is proposed that the pleiotropic phenotype could result from an alteration of the plasma membrane and mitochondrial inner membrane by a single nuclear gene mutation.
Mol Gen Genet 1976 Mar 30
PMID:Some physiological alteration associated with pleiotropic cross resistance and collateral sensitivity in Saccharomyces cerevisiae. 77 99

A procedure was described for the isolation of mutants affected in the regulation of catalase activity. Two such mutants, cgr 1 and cgr 2 were obtained. Both of them show catalase activity that is resistant to repression by glucose, but is sensitive to anoxia to the same extent as the wild type.
Mol Gen Genet 1976 Apr 23
PMID:Haemoprotein formation in yeast. II. Isolation of catalase regulatory mutants. 77 8

This article attempts to trace, from a personal point of view, the history of discoveries of allosteric phenomena in phosphorylase b and the later development of systematic attempts to fit the data into comprehensive theoretical models. Work from our own laboratory is emphasized, but we try to integrate this into the results from other investigators and show their contributions to our ideas and experiments. Finally, some recent unpublished data is presented together with some conclusions and predictions from a new hypothesis. The discoveries by Carl and Gerty Cori of the activation of phosphorylase by AMP, the inhibition of glucose and the enzymatic interconversion of two forms fo the enzyme with different control properties helped lay the foundations of our present understanding of allosteric mechanisms. The later discovery of the oligomeric nature of phosphorylase and its relationship to AMP binding served as a basis for many years of research into the structure-function relationships of phosphorylase and other enzymes. Data showing that AMP lowers the entropy of activation is discussed with respect to the role of the nucleotide and its binding close to the active site. The discovery of the control of phosphorylase b by common metabolites and the impetus this gave to the intensive kinetic studies of the last ten years, wherein fitting to theoretical models has been a common feature, is reviewed.
Mol Cell Biochem 1976 Mar 26
PMID:Studies on allosteric phenomena in glycogen phosphorylase b. 77 16

The formation of ADHII in Saccharomyces cerevisiae is regulated by carbon catabolite repression. There are two genes involved in the formation of ADHII: ADR2, the structural gene as identified by electrophoretic variants and ADR1, possibly a regulatory gene. A new genetic element involved in the regulation of ADHII was identified by three allelic mutants insensitive to strong glucose repression. They were called ADR3c (wild type designation ADR3) and found to be tightly linked to the structural gene, ADR2. The alcohol dehydrogenase found in ADR3c mutants could not be distinguished electrophoretically from the ADHII of the glucose-sensitive wild type, ADR3. Dominance relations between ADR3c and ADR3 were established in diploids heterozygous for ADR3 and the two alleles of ADR2 (ADR2-S: slow ADHII, ADR2-F: fast ADHII). During growth on 10% glucose, an ADR3c adr2-F/ADR3 ADR2-Sheterozygous diploid formed only the fast ADHII variant wheras an ADR3c ADR2-S/ADR3 ADR2-F heterozygote produced only the slow form. This was taken as evidence of the cis-dominance of all ADR3c alleles. The cis-effect of ADR3c was also demonstrated in glucose-derepressed diploids. The ADR3c mutations do not only cause glucose-insensitive ADHII frmation, but also reduce the activity of the adjacent structural gene during derepression. Thus ADR3c alleles were considered to be controlling site mutations. No pleiotropic effects were observed on the formation of enzymes related to the function of ADHII. An adr1 ADR2 ADR3 single mutant did not form ADHII. In contrast to this, an adr1 ADR2 ADR3c double mutant formed ADHII at a similar level as double mutant formed ADHII at a similar level as an ADR1 ADR2 ADR3c mutant. This showed that ADR3c was epistatic over adr1 (previously suggested as a positive regulatory gene). From this it was concluded that ADR1 is the fact a positive regulatory gene the function of which is required for the expression of the structural gene for ADHII, ADR2. ADR3 is the controlling site for the structural gene ADR2. Mutations at this site, ADR3c, alleviate the requirement for the ADR2 gene product. Adr3c is discussed as a promotor or operator site.
Mol Gen Genet 1976 Jun 15
PMID:Cis-dominant regulatory mutations affecting the formation of glucose-repressible alcohol dehydrogenase (ADHII) in Saccharomyces cerevisiae. 78 20

It is shown that caffeine antagonizes petite-induction with ethidium bromide under non-growth conditions when administered during or after mutagenic treatment. Caffeine itself is shown to be a petite-inducing agent when cells are grown in liquid glucose-complete-medium in the presence of the drug. A possible mode of action of caffeine in the ethidium bromide induced petite-mutagenesis is discussed.
Mol Gen Genet 1976 Jul 05
PMID:Effect of caffeine on the rho- -induction with ethidium bromide in Saccharomyces cerevisiae. 78 13


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