Figure 4. Delivery of double-stranded DNA deaminase A (DddA) by B. cenocepacia induces mutagenesis in a subset of resistant recipient species.
(A, D, and G) Mutation frequency as measured by spontaneous rifampicin resistance frequency in clones of different species recovered from growth in competition with B. cenocepacia wild-type or B. cenocepacia dddAE1347A (n = 2). (B, E, and H). Distribution of different mutation types detected in rpoB or the whole genome of rifampicin-resistant clones of different species recovered after growth in competition with wild-type B. cenocepacia. (B) Pattern of spontaneous mutation types observed in rpoB of E.coli derived from Garibyan et al., 2003. (C, F, and I). Genome distribution of different mutation types detected by whole-genome sequencing of rifampicin-resistant clones recovered after competition with B. cenocepacia. Species targeted include E. coli (A–C), E. coli EHEC (D–F), and K. pneumoniae (G–I). Colors relate to Figure 3. Values and error bars reflect mean ± s.d. of n = 2 independent biological replicates with n = 3 technical replicates each. p-values derive from unpaired two-tailed t-test. Spont. Spontaneous.
Figure 4—figure supplement 1. Double-stranded DNA deaminase A (DddA)-mediated intoxication is not mutagenic during competition between B. cenocepacia and certain recipient species.
