Bacteria are extremely adaptable and able adjust their lifestyle very quickly when these changes occur. One dramatic illustration of this capacity is the spread of antibiotic resistance among bacterial pathogens. During the last decade, the emergence of multi-resistant bacteria, which are resistant to several treatments, led to increase mortality caused by common infections. The 2014 report on antimicrobial resistance from the World Health Organization warns against the beginning of a “post-antibiotic” era, when most of the bacterial pathogens will become resistant to all treatments available.
In this context, it is crucial to fully understand the molecular mechanism of bacterial adaptability to ultimately target and limit this ability. To survive in a changing environment, bacteria have to resist to stresses induced by these changes and ultimately to adapt their lifestyle if these changes persist. These two processes are almost contradictory since the first aims at maintaining cell integrity while the second allows long term variability through the acquisition of new traits.
In this project, we wanted to understand how DNA can be uptaken and recombined in the bacterial genome during bacterial transformation. Natural genetic transformation, first discovered in Streptococcus pneumoniae by F. Griffith in 1928, is observed in many Gram-negative and Gram-positive bacteria. This process promotes genome plasticity and adaptability. In particular, it enables many human pathogens such as Streptococcus pneumoniae, Neisseria gonorrhoeae or Vibrio Cholerae to acquire resistance to antibiotics and/or to escape vaccines through the binding and incorporation of new genetic material. While it is well established that this process requires the binding, internalization of external DNA and its recombination in the bacterial genome, the molecular details of these steps are unknown.
