Comparison of genetic variation in healthy and diseased populations of the old-field grass Andropogon virginicus

Background/Question/Methods

Wild plant populations are commonly afflicted by disease, but the prevalence can vary among populations. Some populations may exhibit epidemic levels of disease while other populations of the same host plant species appear disease-free. One possible contribution to variation in prevalence is the genetic structure of the host plant populations. Populations that are more  genetically homogeneous should be more likely to become diseased, for two reasons. First, a pathogen that can successfully infect a very common plant genotype will spread easily among those abundant, common genotypes. Second, a pathogen should be able to more easily evolve virulence in a population with fewer different genotypes. We tested this idea for healthy and infected populations of Andropogon virginicus (broomsedge), a common old-field grass in the eastern U.S, where only about 50% of populations are infected with the smut fungus Sporisorium ellisii. We did PCR for ISSR markers, on 20 individuals each from three healthy and three infected populations. We extracted DNA with DNeasy spin columns by Qiagen, from greenhouse plants grown from field-collected seed. Every test plant had a different seed mother. We calculated percent polymorphic loci and Nei’s gene diversity for each population, using methods for dominant markers.  

Results/Conclusions

Sporisorium ellisii  has strong negative consequences for A. virginicus;  it eliminates reproduction and increases mortality. In addition to our expectation of disease developing in host populations with lower genetic variation, these negative effects could also result in decreased variation. However, our results did not show this pattern. Percent polymorphism ranged from 33-67% in the healthy populations and 42-50%  in the infected populations, with no significant difference between the means for healthy (50%) and infected (47%) populations. Similarly, gene diversity ranged from 0.10-0.15 in the healthy populations and 0.08-0.16 in the diseased populations, again with no significant difference between the means (healthy = 0.12, diseased = 0.11). This suggest that infection of A. virginicus populations by the smut fungus S. ellisii is not related to host genetic variation. There are a number of possible explanations.  First, these results are based on 11 polymorphic markers; addition of more populations and markers  will provide more information. Second, ISSRs provide a genetic fingerprint across the entire genome and are not focused on specific disease resistance genes, which could exhibit different patterns of genetic structure. Third, environmental variables may be the stronger drivers of disease development in this system.