Wednesday 14 December 2022

Understanding biofilms: The life and death of an 'altruistic' bacterium

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A new study from the University of Montreal shows how some bacteria living in a biofilm sacrifice themselves to ensure the survival of the community.


Living in a biofilm provides numerous advantages to bacteria: things like resource sharing, shelter from predators, and increased resistance to toxic compounds such as antibiotics. Yet the option to leave the biofilm when environmental conditions deteriorate can also be of benefit to bacteria, allowing them to relocate to a more hospitable environment.



For the bacterium Caulobacter crescentus, the biofilm becomes a kind of prison in perpetuity: once cells are attached to a surface through a strong adhesive at one end of the cell, they cannot leave the biofilm. However, when these attached cells divide, their unattached 'daughter' cells have a choice of joining the biofilm or moving away.


Caulobacter crescentus is a Gram-negative, oligotrophic bacterium widely distributed in fresh water lakes and streams. The bacterium has a characteristic crescent shape. Caulobacter was the first asymmetric bacterium shown to age. Reproductive senescence was measured as the decline in the number of progenies produced over time.


What is of interest to microbiologists is with how cells decide to stay or leave the biofilm. When Caulobacter cells die in the biofilm, they release their DNA, which inhibits daughter cells from joining the biofilm, hence promoting relocation from environments where death rate increases.


The researchers have set out to determine if cell death occurred randomly as the environmental quality declined or if it was a regulated process responding to a specific signal. This reveals that Caulobacter uses a programmed cell death mechanism that causes some cells to sacrifice themselves when the conditions inside the biofilm deteriorate. This is known as a toxin-antitoxin system.


The mechanism uses a toxin that targets a vital function and its associated antidote, the antitoxin. The toxin is more stable than the antitoxin and when programmed cell death is initiated, the amount of antitoxin is reduced, resulting in cell death. The toxin-antitoxin system is activated when oxygen becomes sparse as the biofilm becomes larger and cells compete for the available oxygen.


The resulting death of a subset of cells releases DNA, which promotes the dispersal of new cells to potentially more hospitable environments, thereby preventing overcrowding that would further reduce environmental quality in the biofilm.


The reference is:


Cecile Berne, Sebastien Zappa, Yves V Brun. eDNA-stimulated cell dispersion from Caulobacter crescentus biofilms upon oxygen limitation is dependent on a toxin-antitoxin system. eLife, 2022; 11 DOI: 10.7554/eLife.80808

Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (

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