Harleen Tewatia, “Evolution of Mucoidy under Phage and Antibiotic Selection”
Mentor: Alita Burmeister, Biological Sciences, Letters & Science (College of)
Poster #189
Bacteriophages (‘phages’) are viruses that infect bacteria and are potential alternatives to antibiotics. One defense mechanism that Escherichia coli has against bacteriophages is the production of exopolysaccharides, resulting in the mucoid phenotype. We previously isolated mucoid mutants, and we found that they are resistant to phage U136B and the antibiotic clindamycin. However, other non-mucoid phage resistance mutations can lead to decreased clindamycin resistance. We hypothesized that simultaneous selection with clindamycin and phage U136B will drive the evolution of the mucoid phenotype. To test this, we performed a 5-day evolution experiment with four treatments: 1) Bacteria only, 2) Bacteria + Phage, 3) Bacteria + Phage + Clindamycin, 4) Bacteria +Clindamycin (N = 10 per treatment, for 40 total populations). We predicted that bacteria evolved with both clindamycin and phage (Treatment #3) will have faster rates of mucoid evolution. Consistent with this hypothesis, we have preliminarily found that mucoid mutants appear by Day 1 in Treatment #3 (5/10 populations). In our ongoing work, we are quantifying the evolution of mucoid mutants in terms of timing and frequency across treatments. We will also test the prediction that clindamycin will slow the evolution of phage resistance. In future work, we will test if populations evolved in the presence of phage will have higher levels of antibiotic resistance. We will also test if evolution produces novel genetic mutations for mucoid-based phenotypes.