General principles for the formation and proliferation of a wall-free (L-form) state in bacteria
- Newcastle University, United Kingdom
Abstract
The peptidoglycan cell wall is a defining structural feature of the bacterial-kingdom. Curiously, some bacteria have the ability to switch to a wall-free or 'L-form' state. Although known for decades, the general properties of L-forms are poorly understood, largely due to the lack of their systematic analysis in the molecular biology era. Here we show that inhibition of the peptidoglycan precursor synthesis promotes the generation of L-forms from both Gram-positive and Gram-negative bacteria. We show that L-forms generated have in common a mechanism of proliferation involving membrane blebbing and tubulation, which is dependant on an altered rate of membrane synthesis. Crucially, this mode of proliferation is independent of the essential FtsZ-based division machinery. Our results suggest that the L-form mode of proliferation is conserved across the bacterial-kingdom, reinforcing the idea that it could have been used in primitive cells, and opening up its use in the generation of synthetic cells.
Article and author information
Author details
Copyright
© 2014, Mercier et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Metrics
-
- 6,430
- views
-
- 978
- downloads
-
- 100
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
A two-part list of links to download the article, or parts of the article, in various formats.
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
General principles for the formation and proliferation of a wall-free (L-form) state in bacteria
eLife 3:e04629.
https://doi.org/10.7554/eLife.04629
Further reading
-
Some bacteria can survive and thrive despite not having a cell wall.
-
- Cell Biology
Multiple gut antimicrobial mechanisms are coordinated in space and time to efficiently fight foodborne pathogens. In Drosophila melanogaster, production of reactive oxygen species (ROS) and antimicrobial peptides (AMPs) together with intestinal cell renewal play a key role in eliminating gut microbes. A complementary mechanism would be to isolate and treat pathogenic bacteria while allowing colonization by commensals. Using real-time imaging to follow the fate of ingested bacteria, we demonstrate that while commensal Lactiplantibacillus plantarum freely circulate within the intestinal lumen, pathogenic strains such as Erwinia carotovora or Bacillus thuringiensis, are blocked in the anterior midgut where they are rapidly eliminated by antimicrobial peptides. This sequestration of pathogenic bacteria in the anterior midgut requires the Duox enzyme in enterocytes, and both TrpA1 and Dh31 in enteroendocrine cells. Supplementing larval food with hCGRP, the human homolog of Dh31, is sufficient to block the bacteria, suggesting the existence of a conserved mechanism. While the immune deficiency (IMD) pathway is essential for eliminating the trapped bacteria, it is dispensable for the blockage. Genetic manipulations impairing bacterial compartmentalization result in abnormal colonization of posterior midgut regions by pathogenic bacteria. Despite a functional IMD pathway, this ectopic colonization leads to bacterial proliferation and larval death, demonstrating the critical role of bacteria anterior sequestration in larval defense. Our study reveals a temporal orchestration during which pathogenic bacteria, but not innocuous, are confined in the anterior part of the midgut in which they are eliminated in an IMD-pathway-dependent manner.
