The survival of individual organisms facing stress is enhanced thanks to the induction of a set of changes. As the intensity, duration and nature of stress is highly variable, the optimal response to stress may be vary from cyclic to unpredictable. Phenotypic heterogeneity may ensure that at least a subset of cells would survive the current stress. In bacteria, this may be achieved in different ways with different consequences, but typically involving illegitimate or homologous recombination on the chromosome. We have therefore developed bioinformatic approaches aiming at detecting either illegitimate or homologous recombination hotspots. We present evidence in favour of a potential for change by illegitimate recombination among stress response genes in E. coli, which may favour the appearance of mutator phenotypes. On the other hand, bacteria that are human pathogens are also faced to frequent stresses caused by the immune system, for which "semi-programmed" evolutionary schemes have been shown to be adaptive. Hence, we explored the potential of intra-chromosomal recombination as basis of many of these strategies and apply exhaustive analysis of recombination hotspots in complete bacterial genomes. Results show that among close bacteria, such as the Mycoplasma, there is a very diverse use of antigenic variation strategies, which can be related with the functional characteristics of immunodominant proteins, and the stresses bacteria face. These different strategies have important consequences on the organization of the chromosomes, as revealed by the average length of operons, intensity of strand bias and selection against inverted repeats.
