Biomedical subjects

L Vitković

Publications and source records attributed to L Vitković.

25 records · Page 2Linked to original sources

PubMed1987

Bacillus subtilis Lyt+ and Lyt- strains secrete peptidoglycan hydrolases.

The phenotypes characteristic of the pleiotropic lytic-deficient Bacillus subtilis mutants have been attributed to reductions in N-acetyl-muramoyl-L-alanine amidase (EC 3.5.1.28) and endo-beta-N-acetyl-glucosaminidase (EC 3.2.1.30). It is reported here that these peptidoglycan hydrolases are secreted. The FJ3 (lyt-1), FJ6 (lyt-2), and Ni15 (lyt-15) mutants secreted the enzymes in amounts comparable to a Lyt+ strain. Thus, the Lyt- mutants appear not be as deficient in the enzymes' synthesis as their cell-bound activities indicated. Based on the levels of cell-bound and extracellular activities measured during growth, it is suggested that the Lyt- phenotype may be due to a deficiency of the enzymes' acceptor(s) in cell walls.

Acetylglucosaminidase↗

PubMed1987

Wall turnover deficiency of Bacillus subtilis Ni15 is due to a decrease in teichoic acid.

Bacillus subtilis Ni15 is deficient in cell wall turnover. The deficiency is removed if the medium contains 0.2 M NaCl, which does not affect growth. The levels of amidase and glucosaminidase, the most likely enzymes involved in turnover, were, in stationary phase Ni15 cells, similar to those in late-exponential phase cells of a standard strain. The Ni15 enzymes were not salt sensitive. However, the Ni15 walls contained 4.7-fold less phosphorus than the walls of the standard strain. Since the phosphorus content of B. subtilis walls reflects the level of teichoic acid, it is proposed that the turnover deficiency of this strain is due to a decrease in wall teichoic acid.

Acetylglucosaminidase↗

PubMed1984

Absence of correlation between rates of cell wall turnover and autolysis shown by Bacillus subtilis mutants.

Bacillus subtilis mutants with reduced rates of cell wall autolysis reached a constant rate of wall turnover after a longer lag than the standard strain but eventually showed the same turnover rate. In reverse, a turnover-deficient mutant autolysed at a slightly higher rate than the standard strain. Consequently, there is no correlation between the rates of cell wall turnover and autolysis.

Bacillus subtilis↗

PubMed1983

Rates of peptidoglycan turnover and cell growth of Bacillus subtilis are correlated.

Peptidoglycan turnover was measured by the decrease of trichloroacetic acid-precipitable label in cells labeled with N-acetyl-D-[14C]glucosamine. The rate of turnover was reduced strongly by the inhibition of RNA or protein synthesis and weakly by the inhibition of lipid, peptidoglycan, or DNA synthesis. It increased with the growth rate (which was controlled by the concentration of oxomethylvalerate limiting the intracellular isoleucine supply) to the same degree in stringent (rel+) and isogenic relaxed (relA) strains. In these and all other strains tested, the turnover rate (k) increased with the growth rate (g) according to the equation, k = 0.70 X g1.38, even when the growth rate was systematically altered by changes in the temperature or in the composition of the medium.

Bacillus subtilis↗

PubMed1977

Purification of the extracellular protease of Bacillus licheniformis and its inhibition by bacitracin.

Sporulating cells of Bacillus licheniformis excrete three seryl proteases that are of similar size, 28,000 daltons, but of different charge at pH 6. The peptide antibiotic bactracin is released from the cells at the same time and exists, in part, as a bacitracin-protease complex that is stable throughout chromatographic procedures employed in enzyme purification. However, preextraction of crude protease with CHCl3 and subsequent gel filtration effect separation of the antibiotic and the enzyme. Three purified, bacitracin-free proteases, designated CMC I, CMC II, and CMC III and whose ratios of total activity are 1:3.7:10.3, respectively, are obtained by chromatography on carboxymethyl cellulose. The major component, CMC III, is inhibited by commercial bacitracin at near-physiological concentrations of the antibiotic.

Bacillus↗

PubMed1977

In vitro production of bacitracin by proteolysis of vegetative Bacillus licheniformis cell protein.

The action of a sporulation-specific seryl protease on antibiotic-free extracts of Bacillus licheniformis cells yields a peptide that is identified as bacitracin by its biological activity, its spectral properties, and its comigration with genuine bacitracin in both paper and thin-layer chromatography. During proteolysis, a chemical structure is generated with the spectral properties of a delta-2 thiazoline ring. The yield in vitro, 4 microgram of bacitracin per mg of protein, is less than the maximal yield from sporulating cells, 75 microgram of bacitracin per mg of cell protein, but is a linear function of the amount of protein in the reaction system. Approximately 30% of the protein yielding the antibiotic is ribosomal associated, and only 25% of that amount can be removed by washing with 1 M NH4Cl. The substrate protein is a constant fraction of the cell protein throughout exponential growth and very early sporulation stages of culture development.

Bacillus↗

PubMedDate not supplied

Cytokines in the central nervous system: regulatory roles in neuronal function, cell death and repair.

Recent evidence suggests that neurons and glia can synthesize and secrete cytokines, which play critical roles in maintaining homeostasis in the central nervous system (CNS) by mediating the interaction between cells via autocrine or paracrine mechanisms. Circulating cytokines and soluble receptors also regulate neuronal function via endocrine mechanisms. Disturbance of the cytokine-mediated interaction between cells may lead to neuronal dysfunction and/or cell death and contribute to the pathogenesis of the CNS diseases (e.g., ischemia, Alzheimer's disease and HIV encephalopathy). Defining the molecular pathways of cytokine dysregulation and neurotoxicity may help to elucidate potential therapeutic interventions for many devastating CNS diseases.

Animals↗