Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The basis for disruption of morphogenesis by depletion of pyridoxine derivatives was studied using a pdxH null mutant of Escherichia coli K-12. Removal of pyridoxal from growing cultures severely inhibited murein synthesis in vivo, whereas simultaneous supplementation with D-alanine effectively prevented inhibition. Extractable alanine racemase was low following such starvation. Selection of mutants overcoming the glycine- or temperature-sensitivity imposed by pyridoxine limitation yielded a variety of phenotypes. The most effective of these extragenic suppressors conferred an elevated alanine racemase activity which was resistant to the effects of pyridoxal removal.
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PMID:Temperature-sensitive murein synthesis in an Escherichia coli pdx mutant and the role of alanine racemase. 306 37

The mazEF locus of Escherichia coil located in an operon together with the upstream relA gene (encoding ATP:GTP 3'-pyrophosphotransferase; (p)ppGpp synthetase), encodes an antitoxin/toxin system which might play a role in programmed cell death under stress and starvation conditions at high cell densities. By homology searches, chromosomally encoded orthologous systems were identified in a variety of bacteria, sometimes without the MazE-like antitoxin, and several bacterial species possess multiple MazEF-like systems (paralogs). In many gram positive bacteria, the mazEF-locus is located directly upstream of the sigB (stress sigma factor sigmaB) operon in a putative operon together with the upstream dal (aIr) gene (encoding D-alanine racemase). The acidic antitoxins are less conserved than the basic toxins. The differences in genomic organization of the mazEFloci in E. coli versus those in gram positive bacteria might indicate their association with different stress response regulons in these organisms. A study on the sigmaB operon of Staphylococcus aureus showed that the mazF gene of this organism is cotranscribed with the sigmaB operon in response to heat shock, providing the first example that the expression of the mazEFlocus might be indeed associated with stress responses.
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PMID:Occurrence of mazEF-like antitoxin/toxin systems in bacteria. 1094 59

A stable mutant of Lactobacillus plantarum deficient in alanine racemase (Alr) was constructed by two successive homologous recombination steps. When the mutant was supplemented with D-alanine, growth and viability were unaffected. Surprisingly, deprivation of d-alanine during exponential growth did not result in a rapid and extensive lysis as observed in Alr-deficient strains of Escherichia coli or Bacillus subtilis. Rather, the starved mutant cells underwent a growth arrest and were gradually affected in viability with a decrease in colony forming units over 99% in less than 24 h. Additionally, fluorescent techniques demonstrated a loss of cell envelope integrity in the starved cells. Prolonged d-alanine starvation resulted in cells with an aberrant morphology. Scanning and transmission electron microscopy analyses revealed an increase in cell length, deficiencies in septum formation, thinning of the cell envelope and perforation of the cell wall in the septum region. We discuss the involvement of peptidoglycan hydrolases in these phenotypic defects in the context of the crucial role played by D-alanine in peptidoglycan biosynthesis and teichoic acids substitution.
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PMID:Knockout of the alanine racemase gene in Lactobacillus plantarum results in septation defects and cell wall perforation. 1504 79

This study focused on the alanine racemase gene (alr-2), which is involved in the synthesis of d-alanine that forms the backbone of the cell wall. A stable alr-2 knockout mutant of Aeromonas hydrophila HBNUAh01 was constructed. When the mutant was supplemented with d-alanine, growth was unaffected; deprivation of d-alanine caused the growth arrest of the starved mutant cells, but not cell lysis. No alanine racemase activity was detected in the culture of the mutant. Additionally, a membrane permeability assay showed increasing damage to the cell wall during d-alanine starvation. No such damage was observed in the wild type during culture. Scanning and transmission electron microscopy analyses revealed deficiencies of the cell envelope and perforation of the cell wall. Leakage of UV-absorbing substances from the mutants was also observed. Thus, the partial viability of the mutants and their independence of d-alanine for growth indicated that inactivation of alr-2 does not impose an auxotrophic requirement for d-alanine.
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PMID:Knockout of the alanine racemase gene in Aeromonas hydrophila HBNUAh01 results in cell wall damage and enhanced membrane permeability. 2604 May 90