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Tryptophanless death in Bacillus subtilis.

I Majerfeld, S Barlati, O Ciferri

    Journal of Bacteriology
    |February 1, 1970
    PubMed
    Summary
    This summary is machine-generated.

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    Bacillus subtilis tryptophan starvation causes cell death, but this can be prevented by other amino acid starvation or chloramphenicol. Tryptophan analogues also prevent death and aid recovery, suggesting the phenomenon isn't simply "tryptophanless death".

    Area of Science:

    • Microbiology
    • Molecular Biology
    • Bacterial Physiology

    Background:

    • Actively growing Bacillus subtilis cultures, specifically tryptophan arginine auxotrophs, exhibit a loss of colony-forming ability upon tryptophan removal.
    • This phenomenon, initially termed "tryptophanless death," requires further investigation into its underlying mechanisms and preventative factors.

    Purpose of the Study:

    • To investigate the phenomenon of cell death in Bacillus subtilis following tryptophan starvation.
    • To determine the factors that prevent or reverse this loss of viability.
    • To clarify the nature of the cellular response to tryptophan deprivation.

    Main Methods:

    • Culturing Bacillus subtilis tryptophan arginine auxotrophs under conditions of tryptophan starvation.
    • Assessing colony-forming ability to quantify cell viability.

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  • Administering various agents, including other amino acids, chloramphenicol, actinomycin, and tryptophan analogues, to observe their effects.

    • Main Results:

    • Tryptophan starvation in actively growing Bacillus subtilis led to a decline in colony-forming ability.
    • This decline was prevented by simultaneous starvation of another essential amino acid or by bacteriostatic concentrations of chloramphenicol.
    • Actinomycin did not prevent the cell death, but tryptophan analogues not only prevented death but also facilitated recovery of colony-forming ability.
    • Chloramphenicol, unlike actinomycin, inhibited the recovery induced by tryptophan analogues.

    Conclusions:

    • The term "tryptophanless death" is inappropriate given that recovery is possible and the phenomenon can be prevented by factors other than tryptophan.
    • The observed cell death is a complex process influenced by multiple cellular conditions and requires protein synthesis inhibition (chloramphenicol) for recovery, but not transcription inhibition (actinomycin).
    • Tryptophan analogues play a significant role in both preventing cell death and promoting recovery, indicating a more nuanced response to amino acid imbalance than previously assumed.