Article Abstract – Hollowell et al. (2016a)
Epidemic Spread of Symbiotic and Non-Symbiotic Bradyrhizobium Genotypes Across California
Authors and affiliations:
A. C. Hollowell1, J. U. Regus1, K. A. Gano1, R. Bantay1, D. Centeno1, J. Pham1, J.Y. Lyu1, D. Moore1, A. Bernardo1, G. Lopez1, A. Patil1, S. Patel1, Y. Lii1, and J. L. Sachs1,2
1Department of Biology and 2Institute for Integrative Genome Biology, University of California, Riverside
Microbial Ecology 71: 700-710 (2016)
The patterns and drivers of bacterial strain dominance remain poorly understood in natural populations. Here, we cultured 1292 Bradyrhizobium isolates from symbiotic root nodules and the soil root interface of the host plant Acmispon strigosus across a >840-km transect in California. To investigate epidemiology and the potential role of accessory loci as epidemic drivers, isolates were genotyped at two chromosomal loci and were assayed for presence or absence of accessory “symbiosis island” loci that encode capacity to form nodules on hosts. We found that Bradyrhizobium populations were very diverse but dominated by few haplotypes—with a single “epidemic” haplotype constituting nearly 30% of collected isolates and spreading nearly statewide. In many Bradyrhizobium lineages, we inferred presence and absence of the symbiosis island suggesting recurrent evolutionary gain and or loss of symbiotic capacity. We did not find statistical phylogenetic evidence that the symbiosis island acquisition promotes strain dominance and both symbiotic and non-symbiotic strains exhibited population dominance and spatial spread. Our dataset reveals that a strikingly few Bradyrhizobium genotypes can rapidly spread to dominate a landscape and suggests that these epidemics are not driven by the acquisition of accessory loci as occurs in key human pathogens.
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