How Bacteria Battle

Upon detecting an incoming attack from the red strain of E. coli, cells of the bottom strain pass this information on to others in the colony, leading to a massive collective attack against the red strain. Green indicates toxin production in the bottom strain.

Despoina Mavridou

Bacteria live in dense communities, where being aware of—and reacting to—the activity in the cells around them is key to survival. They produce an arsenal of toxins that they use, at varying levels of aggression, against competitors. The toxins are well-studied, but how they are deployed is not. A recent series of experiments pitted competing strains of the bacteria Escherichia coli against each other to examine their respective warfare strategies.

An interdisciplinary team of researchers at the University of Oxford focused on a group of toxins, known as colicins, whose production is controlled by a regulatory system that detects damaged DNA—often a symptom of attack by a competitor. Researchers established that thirteen different strains of colicin-producing E. coli—when grown near an E. coli strain that does not make the same toxin—spontaneously manufacture colicin that can restrict the competitor’s growth, thus launching a pre-emptive strike. Upon closer examination, the team found that the individual bacteria cells that disintegrate to release colicins are both more likely to be undergoing DNA damage repair and less likely to reproduce, which means the bacterial colony tends to sacrifice in battle those cells with lower evolutionary fitness.

The team also observed that certain strains generated forms of colicin at higher and more potent levels while in this pre-emptive attack mode. Furthermore, the toxin’s presence had a ripple effect, causing neighboring cells to start pumping out their own colicin and amplifying a colony’s overall toxin production in a response known as autoinduction. Some E. coli strains could not only sense competing colonies’ attacks—and ramp up colicin production and release in response—but also spread this warning to neighboring cells in their colony that had not yet been attacked and rally them to make their own toxin for battle. In this way, such strains could launch massive counter-attacks, collectively reacting to an attack in a way that had never before been seen in bacteria. 

The senior author on the study, evolutionary biologist Kevin Foster, observed, “It looks so much like alarm calling in animals. This is a sophisticated strategy that allows cells to mount a collective reciprocal attack when they are threatened in the same way that honeybees and other social animals do." (Current Biology)