Bacteria produce toxins which kill other bacteria, called bacteriocins. Close relatives of the toxin-producing bacteria have a gene which gives them immunity from the toxin. This means all the clones of the bacteria are safe, but other colonies can still become casualties of microbial warfare. Pretty clever eh?
However like a poorly regulated poker game, cheats are bound to arise. If you manage to evolve an immunity gene without having the gene producing the toxin, then you get all the benefit without the cost. So then there’s an advantage to gaining a new toxin. This can lead to an “arms race” situation, where an array of toxins are produced, in an attempt to one-up the competition and gain an advantage in microbial battle.
Studies in the lab have confirmed this arms race scenario. The problem with lab studies is that we don’t really know what’s going on in nature, and at what scale. My project aimed to identify this. I looked at Pseudomonas fluorescens, a common bacteria you’ll find in the soil (it’s probably lingering in your local park – that’s where all of my samples came from!), to see if there was any evidence of co-evolution occuring in natural populations.
I headed over to my local park and took soil samples along a transect at 0, 1cm, 10cm, 1m and 10m distances. Then I isolated colonies of P.fluorescens and tested them at each distance against each other, to see if they would interfere with each other’s growth through toxin production. I found that at 10cm the most growth inhibition occurred, forming a bell curve shape, which is what theory predicts. My experiments support the idea that microbial warfare is going on in nature, and that for P. fluorescens, the point of most inhibition of growth is 10cm apart from each other – not close enough for there to be much pressure to evolve an immunity gene but not far away enough for there to be no need to produce toxins, an energetically demanding process for the bacteria.
Another cool thing about these toxins is that they are one of the few examples of spite seen in nature – they harm both the bacterium producing the toxin (it is energetically demanding and can kill the bacterium) and the bacteria killed by the toxins are obviously harmed too! It seems that the benefit to clones of the bacterium – its very close relatives – enables spite to exist. By sacrificing itself and killing off non-relatives, the bacteria creates less competition for its clones, meaning their (and therefore the toxin-producing) genes will reach the next generation(s).
This kind of work also has medical applications – a related species – P. aeruginosa infects the lungs of people with Cystic Fibrosis and can be very damaging. The amount of damage it causes – it’s virulence- can vary a lot with these kind of interactions between bacteria. Understanding them helps us understand how infections progress over time, and how we can reduce virulence in these infections.