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. Author manuscript; available in PMC: 2020 Jun 21.
Published in final edited form as: ACS Synth Biol. 2019 May 22;8(6):1249–1256. doi: 10.1021/acssynbio.9b00122

Figure 2—

Figure 2—

(A) Design of experiments tracing source of incompatibility between p1 plasmid replication and r+ strains containing mtDNA and full mitochondrial function. A p1 plasmid with or without TA genes encoded were transferred to r0 (F102–2) or r+ (BY4741) strains and passaged in media that either suppressed (blue) or activated (orange) the toxin phenotype. (B) Stability of p1/p2 in experimental conditions described in (A) after passaging. Agarose gel electrophoresis on DNA extracted from technical triplicates of experiments outlined in (A) show the presence of the expected p1 plasmid in all conditions except for the condition where TA is encoded and activated in a r+ strain. The 2μ plasmid is native to the BY4741-derived strains.