Abstract

Oak wilt is a fungal tree disease that has killed millions of live oaks (Quercus fusiformis Small) in the oak woodlands of central Texas. Allozymes were used to characterize the genetic structure of live oak populations prior to infection (pre-epidemic) and following passage of an epidemic wave (post-epidemic). Pre-epidemic trees (N = 112) were sampled along transects in front of an expanding disease front. Post-epidemic trees (N = 109) were survivors of an epidemic that swept through an area of approximately 28 ha over a period of 20 years. Significant differences in allele and genotype frequencies existed between pre- and post-epidemic populations. Gene diversity was lower for two of the four allozyme loci in the post-epidemic population. Departures from Hardy-Weinberg equilibria occurred for two loci and multilocus associations developed in the post-epidemic population. These results demonstrate that disease can have a significant impact on the genetic structure of a natural host population. We hypothesize that selection for increasing disease resistance was the dominant evolutionary force leading to genetic change in this plant pathosystem.Key words: host-pathogen interactions, population genetics, Ceratocystis fagacearum, coevolution.

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