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Mannitol sensitivity.

P Jensen, C Parkes, D Berkowitz

    Journal of Bacteriology
    |August 1, 1972
    PubMed
    Summary
    This summary is machine-generated.

    Adding mannitol to Salmonella typhimurium mutants lacking mannitol-1-phosphate dehydrogenase causes cell stasis or lysis. This occurs due to intracellular mannitol-1-phosphate accumulation and subsequent lipid synthesis inhibition.

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    Area of Science:

    • Microbiology
    • Cell Biology
    • Biochemistry

    Background:

    • Salmonella typhimurium is a model organism for studying bacterial physiology.
    • Mannitol metabolism is crucial for bacterial energy production and cell integrity.
    • Defects in metabolic pathways can lead to significant cellular dysfunction.

    Purpose of the Study:

    • To investigate the physiological consequences of mannitol-1-phosphate dehydrogenase deficiency in Salmonella typhimurium.
    • To elucidate the impact of intracellular mannitol-1-phosphate accumulation on bacterial cells.
    • To determine the specific cellular processes affected by this metabolic perturbation.

    Main Methods:

    • Culturing Salmonella typhimurium mutants lacking mannitol-1-phosphate dehydrogenase.
    • Supplementing cultures with mannitol and observing cellular responses (stasis, lysis).

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  • Measuring intracellular mannitol-1-phosphate concentrations.
  • Assessing the incorporation of radiolabeled acetate into lipids and other macromolecules.

    • Main Results:

    • Addition of mannitol induced stasis or lysis in the deficient mutants.
    • Intracellular accumulation of mannitol-1-phosphate reached high concentrations (20 mm).
    • Acetate incorporation into lipids was significantly inhibited prior to major impacts on cell wall, protein, or nucleic acid synthesis.

    Conclusions:

    • Mannitol-1-phosphate dehydrogenase is essential for managing mannitol metabolism in Salmonella typhimurium.
    • Excessive intracellular mannitol-1-phosphate accumulation is detrimental, leading to cell death.
    • Lipid synthesis is a primary target affected by this metabolic imbalance, preceding other major cellular processes.