Chloe Skinner, “Bacterial Strain Specificity in the Evolution of Mucoid Phage Resistance”
Mentor: Alita Burmeister, Biological Sciences
Poster #170
Phage-resistance mutations occur rapidly in bacteria, preventing phage infection. One mutant phenotype we study, called mucoid, is also a virulence factor that may limit the ability of phages to be used as therapeutic alternatives to antibiotics. In our previous work, mucoid mutants evolved from Escherichia coli K-12 were selected for using phage U136B. These isolates show resistance through mutations in genes encoding the Rcs Phosphorelay pathway. This pathway is activated through a stress response at the cell membranes and wall, resulting in mucoid capsule regulation. However, we do not yet know if and how other E. coli strains can evolve mucoid resistance. To test this, we are investigating the variation of the mucoid frequency in different laboratory strains with two separate phages, U136B and P1. We used plate-based selection experiments and screened for the mucoid phenotype using E. coli B and K-12 with phages P1 and U136B. We also tested cross resistance of our U136B-resistant, K-12 mucoid mutants on P1 phage using the cross-streak method. We found that mucoid mutants of E. coli K-12 appear under P1 selection (4/28 replicates, 14%) but at a lower frequency than under U136B (35/110 replicates, 32%). However, mucoid mutants that are resistant to U136B are also resistant to phage P1. Strikingly, mucoid mutants of E. coli B do not appear under selection by either phage (0/45 P1 replicates, 0/57 U136B replicates). Overall, these results show that mucoid resistance depends on both the host strain and the selecting phage.