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. 2020 Nov 28;38(4):1472–1481. doi: 10.1093/molbev/msaa307

Fig. 4.

Fig. 4.

Analysis of the fitness compensatory evolution experiment. (A) Overview over acquisition of mutations that effect the production of ppGpp or c-di-GMP, mutations within LysR-type transcriptional regulators, and mutations in genes that can cause a mutator phenotype. A detailed overview over all acquired mutations is given in supplementary table S5, Supplementary Material online. (B) Potential model for the RelA-SpoT interaction within the hybrids. Acquisition of the mutated donor spoT1 gene (spoT D84 ins QD, H255Y) leads to an overproduction of ppGpp due to reduced ppGpp hydrolysis and a premature entry into stationary phase. Deletion of the relA gene reduces cellular ppGpp levels and restores bacterial fitness. (C–F) Growth curves of the S. Typhimurium recipient strain (TH6767, gray), the four unevolved hybrids T1 (C), T2 (D), T3 (E), and T4 (F) (red), a representative evolved hybrid (T1-1, T2-5, T3-1, and T4-7, blue) and unevolved hybrids with deleted relA gene (black). The improvement in growth caused by the deletion of relA is indicated in green.