The advent of next-gen and whole-genome sequencing is allowing unforeseen advances in evolutionary biology. For the study of symbioses in particular, these approaches are allowing biologists to begin to resolve the genetic mechanisms that drive the origins, maintenance and breakdown of symbiotic interactions. We use genomic data to test evolutionary genetic hypotheses about the different trajectories of bacterial mutualists and pathogens, to reconstruct extremely well-resolved phylogenies and to examine the genomic changes that occur in during evolutionary transitions in host association.

Sachs, J. L. and Bull, J.J. 2005. Experimental evolution of conflict mediation between genomes Proceedings of the National Academy of Sciences 102:390-395. [PDF]

Medina, M. and Sachs, J.L. 2010. Symbiont genomics; Our new tangled bank. Genomics 95:129-137. [PDF]

Sachs, J.L., Skophammer, R.G., and Regus, J.U. 2011. Evolutionary transitions in bacterial symbiosis. Proceedings of the National Academy of Sciences USA. 108: 10800-10807. [PDF]

Sachs, J. L., Essenberg, C. and Turcotte. M. M. 2011 New Paradigms for the evolution of beneficial infections. Trends in Ecology and Evolution. 26: 202-209. [PDF]

Sachs, J. L., Russell, J. E. and Hollowell, A. C. 2011. Evolutionary instability of symbiotic
function in Bradyrhizobium. PLoS One: in press.

The evolutionary origins of uncooperative symbionts

A key prediction for symbioses is that they are evolutionarily unstable: mutants are predicted to arise and spread in symbiont populations that exploit host resources without paying costs to hosts. For instance, rhizobia are bacteria that fix nitrogen in legume roots in exchange for photosynthates from their hosts. Uncooperative rhizobia – including non-fixing and non-nodulating strains – appear common in agriculture, yet their population biology and origins remain unknown in natural soils. In a recent study (Sachs et al. 2010a, below), a phylogenetically broad sample of 62 wild-collected rhizobial isolates was experimentally inoculated onto Lotus strigosus to assess their nodulation ability and effects on host growth.

A cheater strain was discovered that proliferated in host tissue while offering no benefit; its fitness was superior to that of beneficial strains. Phylogenetic reconstruction of Bradyrhizobium rDNA and transmissible symbiosis-island loci suggest that the cheater evolved via a massive symbiotic gene transfer event. Many non-nodulating strains were also identified and it appears that nodulation ability has been recurrently lost in the symbiont population.

Sachs, J.L., Ehinger, E. O., & Simms, E. L. 2010a.  Origins of cheating and loss of symbiosis in wild Bradyrhizobium. Journal of Evolutionary Biology. 23:1075-1089. [PDF]

Sachs, J. L., and Simms, E.L. 2008. The origins of uncooperative rhizobia. Oikos117:961-966. [PDF]

Sachs, J. L., and Simms, E.L. 2006. Pathways to mutualism breakdown. Trends in Ecology and Evolution 21:585-592 [PDF]

Sachs, J. L. and Wilcox, T.P. 2006. A shift to parasitism in the jellyfish symbiont Symbiodinium microadtriaticum. Proceedings of the Royal Society of London, B. 273:425-429. [PDF]

Microecology of environmental and symbiotic bacteria

Symbiotic bacteria often encounter hosts from environmental sources and can exhibit multiple life histories including host-inhabiting and environmental stages. Research on host-associated bacteria -- including pathogens and beneficial symbionts -- has primarily focused on infection of hosts. In the mean time, key questions about the ecology and evolution of free-living stages has remained unanswered. For instance, is host association ubiquitous within bacterial lineages, or do host-infecting genotypes represent subsets of environmental populations? Assuming that host infection and free-living existence exert different selective pressures, do diverged bacterial lineages result? Another set of questions addresses the degree to which bacteria associate with specific host partners. Do bacterial genotypes invariably associate with specific host lineages, and is such specificity based on control by one or both partners? Alternatively, is specificity a byproduct of ecological co-occurrence among bacteria and hosts? We have been using a combination of phylogenetic and population genetic approaches to tackle these questions.

 Sachs, J.L., Kembel, S.W., Lau, A.H., and Simms, E.L.  2009. In situ phylogenetic structure and diversity of wild Bradyrhizobium communities. Applied and Environmental Microbiology 75: 4727-4735. [PDF]

Host control mechanisms are thought to be critical for selecting against cheater mutants in symbiont populations. Some of our recent research has tested a legume host’s ability to constrain the infection and proliferation of a native occurring rhizobial cheater (Sachs et al. 2010b, below). Lotus strigosus hosts were experimentally inoculated with pairs of Bradyrhizobium strains that naturally vary in symbiotic benefit, including a cheater symbiont strain that proliferates in the roots of singly-infected hosts yet provides zero growth benefits. Within coinfected hosts, the cheater exhibited lower infection rates than competing beneficial strains and grew to smaller population sizes within those nodules. In vitro assays revealed that infection-rate differences among competing strains were not due to variation in rhizobial growth rate or inter-strain toxicity. These results can explain how a rapidly growing cheater symbiont – that exhibits a massive fitness advantage in single infections – can be prevented from sweeping through a beneficial population of symbionts.

Simms, E. L., Taylor, D. L., Povich, J., Shefferson, R. P., Sachs, J. L., Urbina, M., and Tauszick, Y. 2006. An empirical test of partner choice mechanisms in a wild legume- rhizobium interaction. Proceedings of the Royal Society of London 273:77-81. [PDF]

Sachs, J.L., Russell, J. E., Lii, Y. E., Black, K. C., Lopez, G., and Patil, A. S. 2010. Host control over infection and proliferation of a cheater symbiont. Journal of Evolutionary Biology. 23:1919-1927. [PDF]