In this study we used molecular techniques to examine deer movement and population structure in the context of chronic wasting disease transmission and spread. Chronic wasting disease is an infectious prion encephalopathy in cervids that is endemic to Colorado and Wyoming but has spread across the US within the last decade. Quantifying white-tailed deer movement and population structure in infected areas can facilitate predictions of CWD spread via deer dispersal. We analyzed microsatellite genotypes of white-tailed deer populations in southern Wisconsin and Illinois to quantify population level movements, genetic admixture and gender-biased dispersal patterns using FST and contingency tests. We also examined movements of individuals using assignment tests and spatial autocorrelation, and quantified dispersal events using parentage assignment. Finally, we compared genetic characteristics such as allelic diversity, heterozygosity and fixation indices between CWD infected and uninfected individuals to determine if CWD affects movement of white-tailed deer. Genetic characteristics were not different between CWD infected and uninfected deer, suggesting that changes in movement behaviors associated with clinical illness were not detectable with our molecular data. We found that both male and female deer move extensively in northern Illinois and southern Wisconsin, and that this movement could facilitate CWD spread via dispersal. In contrast, a few locations demonstrated reduced deer movement and female philopatry. One of these locations is a hotspot for CWD in Illinois, and it appears that reduced movements in this area could be exacerbating CWD transmission via direct contact among deer. The observed spatial heterogeneity in deer movement and population structure has important management implications as it allowed us to identify locations at risk for future CWD infection and areas in need of management.Our study was intented to guide population management and conservation, so we wanted to ensure that biological inferences were based on accurate genetic information. Therefore we identified sources of genotyping errors, evaluated measures to correct for their presence and provided recommendations to prevent their negative impacts. We detected null alleles in five of 13 previously evaluated microsatellites, and redesigned primers for two of these loci. Analytical corrections for null alleles were unable to fully prevent bias associated with these genotyping errors, and consequently, measures of population differentiation and kinship were negatively impacted. Our results demonstrate the importance of error evaluation during all stages of population studies, and emphasize the need to standardize procedures for genetic marker evaluation. Since chronic wasting disease management often involves decreasing deer densities to reduce the likelihood of disease occurrence and spread, we wanted to examine the genetic consequences of management in white-tailed deer herds. Increased removal of individuals can alter genetic characteristics of the population, cause a loss of genetic diversity, a decrease in fitness, or enable increased immigration. We compared allele frequencies among cohorts of deer to determine if culling changed the genetic composition of managed populations. Additionally, allele frequency distributions, heterozygosity, and genetic characteristics such as allelic richness and fixation indices were evaluated in pre- and post-cull deer populations to examine the effects of culling on effective population size, genetic differentiation and genetic diversity of white-tailed deer. Cohorts demonstrated little change in allele frequencies from year to year. However, evaluations of pre- and post-cull populations revealed increases in allelic richness and deficiencies in heterozygosity in post-cull populations, suggesting that these populations have received immigrants following intervention. Moreover, female deer, which tend to be philopatric, had significant changes in allele frequencies after culling was initiated. This study suggests that while reducing deer densities through culling enriches the genetic composition of deer, it could also result in immigration of CWD infected deer, and these potential ecological consequences need to be considered during the implementation of disease management plans. In this investigation, we also used landscape genetics to examine the effect of landscape features on dispersal and population boundaries of white-tailed deer. An awareness of how the landscape affects animal movement and genetic exchange between populations contributes to our understanding of wildlife ecology. By quantifying genetic structure across the landscape we have identified populations with high and low admixture and discovered gender specific barriers to deer movement that may contribute to CWD spread via dispersal. We found that rivers, streams and interstates contributed to the genetic structuring of females in the study area, but males were insensitive to these features. The observed variations in landscape use between males and females implies that CWD could spread via male movement relatively independently of natural and manmade landscape features, while CWD spread by females would occur over shorter distances because movement is inhibited by these landscape features. Certain genotypes of the prion gene (Prnp) have been shown to prolong disease progression and survival of CWD infected deer. Therefore, examining Prnp genotypes in CWD infected and uninfected deer populations can reveal associations between genotype and phenotype to determine if selective pressures are affecting Prnp allele frequencies. If selection is occurring, we would expect Prnp genotypes that prolong survival to be higher in infected populations compared to uninfected populations. To test this hypothesis, we sequenced Prnp of 219 (99 CWD positive and 120 CWD negative) deer from the CWD outbreak region of northern Illinois and southern Wisconsin. We also sampled deer from two uninfected populations: one ~150 km away from the outbreak region, and another ~300 km from the outbreak region. Twelve nucleotide polymorphisms, eight silent and four coding, were found in Prnp of the sampled populations. Five polymorphic loci had significantly different distributions of alleles between infected and uninfected individuals. Nucleotide base changes 60C/T, 285A/C, 286G/A, and 555C/T were observed with higher than expected frequencies in CWD negative animals suggesting disease resistance, while 153C/T was observed more than expected in positive animals, suggesting susceptibility. The total number of polymorphisms per animal, silent or coding, was negatively correlated to disease status. Polymorphisms 243T/A, 286G/A and 555C/T were found at higher than expected frequencies in uninfected populations. The total number of polymorphisms, both silent and coding, also differed between infected and uninfected populations. At the temporal scale examined, selection does not appear to be favoring genotypes associated with CWD resistance as these genotypes tended to have higher frequencies in uninfected populations.
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