Abstract
Two diametric paradigms have been proposed to model the molecular co-evolution of microbial mutualists and their eukaryotic hosts. In one, mutualist and host exhibit an antagonistic arms race and each partner evolves rapidly to maximize their own fitness from the interaction at potential expense of the other. In the opposing model, conflicts between mutualist and host are largely resolved and the interaction is characterized by evolutionary stasis. We tested these opposing frameworks in two lineages of mutualistic rhizobia, Sinorhizobium fredii and Bradyrhizobium japonicum. To examine genes demonstrably important for host-interactions we coupled the mining of genome sequences to a comprehensive functional screen for type III effector genes, which are necessary for many Gram-negative pathogens to infect their hosts. We demonstrate that the rhizobial type III effector genes exhibit a surprisingly high degree of conservation in content and sequence that is in contrast to those of a well characterized plant pathogenic species. This type III effector gene conservation is particularly striking in the context of the relatively high genome-wide diversity of rhizobia. The evolution of rhizobial type III effectors is inconsistent with the molecular arms race paradigm. Instead, our results reveal that these loci are relatively static in rhizobial lineages and suggest that fitness conflicts between rhizobia mutualists and their host plants have been largely resolved.
Highlights
Eukaryotes universally encounter bacteria that inhabit, infect, and often provide them with significant fitness benefits
We demonstrate that the type III effector genes of these rhizobial species are highly conserved in content with little diversity between strains
The type III secretion system is a key mechanism used by a diversity of bacterial mutualists to establish infections with their hosts
Summary
Eukaryotes universally encounter bacteria that inhabit, infect, and often provide them with significant fitness benefits. One common paradigm models mutualisthost interactions as an antagonistic arms race, as is the case for coevolution of pathogens and their hosts Under this model, natural selection is predicted to shape partners to rapidly evolve traits to maximize their own selfish gains from the interaction and minimize costs invoked by the other [1]. The interaction is predicted to exhibit evolutionary stability, with lower rates of evolutionary change Testing these competing frameworks by comparing the genetic patterns of known hostassociation genes between mutualists and pathogens will help to examine whether bacteria-eukaryotic mutualisms represent reciprocally exploitative interactions, as they have often been characterized, or alternatively, if these interactions exhibit a ‘‘mutualistic environment’’ in which evolutionary stasis is maintained [1,3]. Many phytopathogenic bacteria use type III secretion systems (T3SS) to deliver collections of type III effector proteins (T3Es) to dampen host defenses, thereby allowing the bacteria to proliferate
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