I’m currently off on my seriously-delayed honeymoon, so over the next two weeks I’ll be sticking up some posts I enjoyed from my old blog. They’ve been modified and re-edited to include new information (and images!) where appropriate, but unfortunately I won’t be able to answer comments or participate in any discussion about them until I get back.
Although bacteria live as isolated cells they are constantly communicating with surrounding bacteria, particularly those of the same species, and can often band together to form large groups of bacteria surrounded by a sticky mesh. These are known as biofilms (which I cover in more detail here). One of the main ways that bacteria communicate with each other in order to organise structures like this is by quorum sensing.
Quorum sensing uses small molecules that bacteria can both excrete and sense. When enough bacteria are in one place then the surrounding concentration of these small molecules reaches a critical level and can activate the genes for a variety of different responses including luminescence, virulence (in pathogenic or disease-causing bacteria) and the formation of biofilms:
It turns out that there are a whole range of different types of biofilms, that bacteria use for many different purposes. Although many species formed biofilms when bany cells joined together some species stopped forming biofilms when they reached a certain cell density. Biofilms are carefully controlled by bacteria, they do not just start growing when a certain number of bacterial cells gather together and then never stop, each biofilm is tailored specifically to the needs of the species making it.
Using models of mostly infectious biofilm-forming bacteria (such as Vibrio cholerae which causes cholera) they found that as well as helping to bind the cells together and resist attacks from antibiotics the biofilm was also a defense against competing bacteria and may have helped to out-compete them by covering all available living surfaces with slime. The ability to produce biofilms not only helps the V. cholerae against other invading bacteria, it also helps it gain a hold against the body’s own internal bacterial defenses that line the internal gut.
However once the levels of V. cholerae became too high the bacteria often stopped generating the biofilms. This could be for two reasons, firstly the biofilm takes up valuable resources that could be used in growth and division and secondly it prevents the bacteria within it from travelling very far. V. cholerae infect the body by having periods of growth followed by periods of mad colonisation, which works best if the biofilm actually disperses at high cellular density to allow the cells to spread.
This can be contrasted with more sedentary bacteria like P. aeruginosa which likes to settle down once it finds a place to live and occasionally disperse colonies into the body. Rather than loosing its biofilm this bacterial species retains it even at high cell densities. This allows it to out-compete any other bacteria that may be at the site of infection, and hold off both the body’s natural defenses and any chemical antibiotic drugs meant to kill it.
Comparisons of different V. cholerae strains revealed a wide range of different biofilm formation patterns between strains, all linked to Quorum sensing signalling. This is likely to depend on the internal environment that specific strains occupy, the amount of competition they face and the necessity for quick and frequent bouts of dispersal.
Biofilms are often seen as being a final living space, a giant bacterial ‘city-base’ from which offspring can spread while the old-timers stay and develop antibiotic-resistance to new challenges. It’s interesting to see that this is not always the case. That the biofilm can just as easily be a short-term shack for travellers as well as a city for settlers.
Credit for image 1
Reference: Nadell CD, Xavier JB, Levin SA, & Foster KR (2008). The evolution of quorum sensing in bacterial biofilms. PLoS biology, 6 (1) PMID: 18232735