‘Lonely’ bacteria lead to antibiotic resistance

Smaller groups of bacteria are more likely to become resistant to antibiotics than larger groups suggests new research from the University of Manchester. The research, published in Nature Communications, explored mutation rates in E. coli, and revealed smaller groups of microbes are more likely to mutate than larger groups and thus develop a greater resistance to Rifampicin, an antibiotic used to treat tuberculosis. “What we were looking for was a connection between the environment and the ability of bacteria to develop the resistance to antibiotics,” said Dr Chris Knight, joint leader on the study. “We discovered that the rate at which E. coli mutated depends upon how many ‘friends’ it has around. It seems that more lonely organisms are more likely to mutate.” The change in mutation rate is controlled by quorum sensing – a form of social communication which allows bacteria know how much of a crowd there is. It involves the release of signalling molecules by bacteria; the denser the population, the more molecules are released and detected. This enables the bacteria understand their environment and coordinate their behaviour to improve defence mechanisms and adapt to the availability of nutrients. “We were able to change their mutation rates by changing who they shared test-tubes with, which could mean that bacteria manipulate each other’s mutation rates,” said Dr Rok Krašovec, joint study leader. “It also suggests that mutation rates could be affected when bacteria are put at low densities, for instance by a person taking antibiotics.” The rate of mutation was found to depend on the gene luxS, known to be involved in quorum sensing in a wide range of bacteria. The team – who were funded by the Wellcome Trust and the EPSRC – now hope to find ways to control this signalling for medical applications. “Eventually this might lead to interventions to control mutation rates, for instance to minimise the evolution of antibiotic resistance, allowing antibiotics to work better,” said Knight. Mutation rate plasticity in rifampicin resistance depends on Escherichia coli cell–cell interactions