| Autor: |
Grekov I; Department of Molecular Bacteriology, Helmholtz Centre for Infection Research, Braunschweig, Germany.; Department of Clinical Microbiology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark., Thöming JG; Institute of Molecular Bacteriology, TWINCORE Centre for Experimental and Clinical Infection Research, Hannover, Germany.; Department of Clinical Microbiology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark., Kordes A; Institute of Molecular Bacteriology, TWINCORE Centre for Experimental and Clinical Infection Research, Hannover, Germany.; Cluster of Excellence RESIST (EXC 2155), Hannover Medical School, Hannover, Germany., Häussler S; Department of Molecular Bacteriology, Helmholtz Centre for Infection Research, Braunschweig, Germany. Susanne.haeussler@helmholtz-hzi.de.; Institute of Molecular Bacteriology, TWINCORE Centre for Experimental and Clinical Infection Research, Hannover, Germany. Susanne.haeussler@helmholtz-hzi.de.; Department of Clinical Microbiology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark. Susanne.haeussler@helmholtz-hzi.de.; Cluster of Excellence RESIST (EXC 2155), Hannover Medical School, Hannover, Germany. Susanne.haeussler@helmholtz-hzi.de. |
| Abstrakt: |
Identifying genetic factors that contribute to the evolution of adaptive phenotypes in pathogenic bacteria is key to understanding the establishment of infectious diseases. In this study, we performed mutation accumulation experiments to record the frequency of mutations and their effect on fitness in hypermutator strains of the environmental bacterium Pseudomonas aeruginosa in comparison to the host-niche-adapted Salmonella enterica. We demonstrate that P. aeruginosa, but not S. enterica, hypermutators evolve toward higher fitness under planktonic conditions. Adaptation to increased growth performance was accompanied by a reversible perturbing of the local genetic context of membrane and cell wall biosynthesis genes. Furthermore, we observed a fine-tuning of complex regulatory circuits involving multiple di-guanylate modulating enzymes that regulate the transition between fast growing planktonic and sessile biofilm-associated lifestyles. The redundancy and local specificity of the di-guanylate signaling pathways seem to allow a convergent shift toward increased growth performance across niche-adapted clonal P. aeruginosa lineages, which is accompanied by a pronounced heterogeneity of their motility, virulence, and biofilm phenotypes. |
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