Erin E. Rees1, Bruce A. Pond2, Catherine I. Cullingham1, Rowland R. Tinline3, David Ball3, Christopher J. Kyle1, Richard C. Rosatte2, and Bradley N. White1. (1) Trent University, (2) Ontario Ministry of Natural Resources, (3) Queen's University
Landscape barriers have implications for infectious wildlife disease control. Since the quality of disease incidence data can compromise estimates of barrier effects we used neutral genetic markers. We investigated the mechanisms that may prevent gene flow between raccoons in Ontario (ON) and New York (NY) resulting in mitochondrial genetic structure. In this region there is a high risk for raccoon rabies to be entering ON from NY. A stochastic, individual-based, spatial model simulated raccoon population dynamics and the inheritance of the genetic markers. The species range was modelled to expand from NY across the Niagara River into ON over 200 years, using multiple runs for different levels of river permeability to raccoon movement. Every 25 years the genetic population structure was characterised using PhiST, simple and partial Mantel tests and a gene diversity measure. Isolation by distance has previously been observed at larger scales but was not found in this study region for modelled or empirical data. The model did show “founder” genetics to dominate the colonizing population’s structure, and, as the river barrier effect increased, genetic diversity decreased. Comparing simulated and empirical genetic measures, for 166 raccoons sampled in the field from the same landscape, the river was found to reduce movement by 50 - 75 percent; and an even stronger amount on an island not connected by bridges. The results suggest the actual colonisation event occurred 200 to 400 years ago. Including genetics in simulation modelling benefits investigations of species range expansion and disease spread.