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  • Title: Listeria monocytogenes L-forms respond to cell wall deficiency by modifying gene expression and the mode of division.
    Author: Dell'Era S, Buchrieser C, Couvé E, Schnell B, Briers Y, Schuppler M, Loessner MJ.
    Journal: Mol Microbiol; 2009 Jul; 73(2):306-22. PubMed ID: 19555455.
    Abstract:
    Cell wall-deficient bacteria referred to as L-forms have lost the ability to maintain or build a rigid peptidoglycan envelope. We have generated stable, non-reverting L-form variants of the Gram-positive pathogen Listeria monocytogenes, and studied the cellular and molecular changes associated with this transition. Stable L-form cells can occur as small protoplast-like vesicles and as multinucleated, large bodies. They have lost the thick, multilayered murein sacculus and are surrounded by a cytoplasmic membrane only, although peptidoglycan precursors are still produced. While they lack murein-associated molecules including Internalin A, membrane-anchored proteins such as Internalin B are retained. Surprisingly, L-forms were found to be able to divide and propagate indefinitely without a wall. Time-lapse microscopy of fluorescently labelled L-forms indicated a switch to a novel form of cell division, where genome-containing membrane vesicles are first formed within enlarged L-forms, and subsequently released by collapse of the mother cell. Array-based transcriptomics of parent and L-form cells revealed manifold differences in expression of genes associated with morphological and physiological functions. The L-forms feature downregulated metabolic functions correlating with the dramatic shift in surface to volume ratio, whereas upregulation of stress genes reflects the difficulties in adapting to this unusual, cell wall-deficient lifestyle.
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