RESUMO
The processes responsible for the evolution of key innovations, whereby lineages acquire qualitatively new functions that expand their ecological opportunities, remain poorly understood. We examined how a virus, bacteriophage λ, evolved to infect its host, Escherichia coli, through a novel pathway. Natural selection promoted the fixation of mutations in the virus's host-recognition protein, J, that improved fitness on the original receptor, LamB, and set the stage for other mutations that allowed infection through a new receptor, OmpF. These viral mutations arose after the host evolved reduced expression of LamB, whereas certain other host mutations prevented the phage from evolving the new function. This study shows the complex interplay between genomic processes and ecological conditions that favor the emergence of evolutionary innovations.
Assuntos
Proteínas da Membrana Bacteriana Externa/metabolismo , Bacteriófago lambda/genética , Escherichia coli/virologia , Evolução Molecular , Mutação , Porinas/metabolismo , Receptores Virais/metabolismo , Proteínas da Cauda Viral/genética , Alelos , Proteínas da Membrana Bacteriana Externa/genética , Bacteriófago lambda/fisiologia , Escherichia coli/genética , Escherichia coli/metabolismo , Genoma Bacteriano , Genoma Viral , Polimorfismo de Nucleotídeo Único , Porinas/genética , Receptores Virais/genética , Seleção Genética , Proteínas da Cauda Viral/química , Proteínas da Cauda Viral/metabolismoRESUMO
The dynamics of host susceptibility to parasites are often influenced by trade-offs between the costs and benefits of resistance. We assayed changes in the resistance to three viruses in six lines of Escherichia coli that had been evolving for almost 45,000 generations in their absence. The common ancestor of these lines was completely resistant to T6, partially resistant to T6* (a mutant of T6 with altered host range), and sensitive to λ. None of the populations changed with respect to resistance to T6, whereas all six evolved increased susceptibility to T6*, probably ameliorating a cost of resistance. More surprisingly, however, the majority of lines evolved complete resistance to λ, despite not encountering that virus during this period. By coupling our results with previous work, we infer that resistance to λ evolved as a pleiotropic effect of a beneficial mutation that downregulated an unused metabolic pathway. The strong parallelism between the lines implies that selection had almost deterministic effects on the evolution of these patterns of host resistance. The opposite outcomes for resistance to T6* and λ demonstrate that the evolution of host resistance under relaxed selection cannot be fully predicted by simple trade-off models.
