Fig. 1

Extracellular poly(dC) modulates PAO1 persistence. a, b The number of total and persister cells before and after washing (e), (s), or (d) WT cells as well as after resuspending corresponding washed cells in their native supernatants (neutralization). c Persistence in washed (e) WT cells or washed (s) WT cells plus short poly(dC) or P-poly(dC). Poly(dC) instead of P-poly(dC) reduced persistence in washed (e) WT cells and washed (s) WT cells. d Persistence in washed (s) WT cells plus each poly(dC₁₂) mutant, poly(dA₁₂), poly(dT₁₂), or poly(dG₁₂). These ssDNA led to a nearly 10-fold reduction in persistence of washed (s) WT cells. As a control, poly(dC₁₂) caused a more than 100-fold reduction in persistence of washed (s) WT cells. e Persistence in washed (s) WT cells plus poly(dC₁₂) and P-poly(dC₁₂) with different molar ratios. P-poly(dC₁₂) abolished the regulatory activity of poly(dC₁₂) in persistence of washed (s) WT cells. f Persistence in washed (s) WT cells plus poly(dC₁₂) for 10 min and then P-poly(dC₁₂) for 10 min or plus P-poly(dC₁₂) for 10 min and then poly(dC₁₂) for 10 min. P-poly(dC₁₂) did not regulate persistence in poly(dC₁₂)-pretreated washed (s) WT cells and vice versa. g Persistence in washed (s) WT cells plus P-poly(dC₁₂) for 10 min, washing again, and then plus poly(dC₁₂) for 10 min. These treatments did not reduce persistence in washed (s) WT cells. h Proposed model for functional antagonism between poly(dC) and P-poly(dC). All experiments were performed in biological triplicates. Error bars represent standard deviations. Dot plots overlaid on bar graphs represent individual data points. Black spot, treatment step or object; arrow, treatment order