Listeria monocytogenesl-forms respond to cell wall deficiency by modifying gene expression and the mode of division
Article first published online: 23 JUN 2009
© 2009 The Authors. Journal compilation © 2009 Blackwell Publishing Ltd
Volume 73, Issue 2, pages 306–322, July 2009
How to Cite
Dell'Era, S., Buchrieser, C., Couvé, E., Schnell, B., Briers, Y., Schuppler, M. and Loessner, M. J. (2009), Listeria monocytogenesl-forms respond to cell wall deficiency by modifying gene expression and the mode of division. Molecular Microbiology, 73: 306–322. doi: 10.1111/j.1365-2958.2009.06774.x
- Issue published online: 10 JUL 2009
- Article first published online: 23 JUN 2009
- Accepted 11 June, 2009.
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.