Understanding how spatial genetic patterns respond to landscape change is crucial for advancing the emerging field of landscape genetics. We quantified the number of generations for new landscape barrier signatures to become detectable and for old signatures to disappear after barrier removal. We used spatially explicit, individual-based simulations to examine the ability of an individual-based statistic [Mantel's r using the proportion of shared alleles' statistic (Dps)] and population-based statistic (FST ) to detect barriers. We simulated a range of movement strategies including nearest neighbour dispersal, long-distance dispersal and panmixia. The lag time for the signal of a new barrier to become established is short using Mantel's r (1-15 generations). FST required approximately 200 generations to reach 50% of its equilibrium maximum, although G'ST performed much like Mantel's r. In strong contrast, FST and Mantel's r perform similarly following the removal of a barrier formerly dividing a population. Also, given neighbour mating and very short-distance dispersal strategies, historical discontinuities from more than 100 generations ago might still be detectable with either method. This suggests that historical events and landscapes could have long-term effects that confound inferences about the impacts of current landscape features on gene flow for species with very little long-distance dispersal. Nonetheless, populations of organisms with relatively large dispersal distances will lose the signal of a former barrier within less than 15 generations, suggesting that individual-based landscape genetic approaches can improve our ability to measure effects of existing landscape features on genetic structure and connectivity.

The spatial structure of the environment (e.g. the configuration of habitat patches) may play an important role in determining the strength of local adaptation. However, previous studies of habitat heterogeneity and local adaptation have largely been limited to simple landscapes, which poorly represent the multiscale habitat structure common in nature. Here, we use simulations to pursue two goals: (i) we explore how landscape heterogeneity, dispersal ability and selection affect the strength of local adaptation, and (ii) we evaluate the performance of several genotype-environment association (GEA) methods for detecting loci involved in local adaptation. We found that the strength of local adaptation increased in spatially aggregated selection regimes, but remained strong in patchy landscapes when selection was moderate to strong. Weak selection resulted in weak local adaptation that was relatively unaffected by landscape heterogeneity. In general, the power of detection methods closely reflected levels of local adaptation. False-positive rates (FPRs), however, showed distinct differences across GEA methods based on levels of population structure. The univariate GEA approach had high FPRs (up to 55%) under limited dispersal scenarios, due to strong isolation by distance. By contrast, multivariate, ordination-based methods had uniformly low FPRs (0-2%), suggesting these approaches can effectively control for population structure. Specifically, constrained ordinations had the best balance of high detection and low FPRs and will be a useful addition to the GEA toolkit. Our results provide both theoretical and practical insights into the conditions that shape local adaptation and how these conditions impact our ability to detect selection.

Reliable interpretation of landscape genetic analyses depends on statistical methods that have high power to identify the correct process driving gene flow while rejecting incorrect alternative hypotheses. Little is known about statistical power and inference in individual-based landscape genetics. Our objective was to evaluate the power of causal-modelling with partial Mantel tests in individual-based landscape genetic analysis. We used a spatially explicit simulation model to generate genetic data across a spatially distributed population as functions of several alternative gene flow processes. This allowed us to stipulate the actual process that is in action, enabling formal evaluation of the strength of spurious correlations with incorrect models. We evaluated the degree to which naïve correlational approaches can lead to incorrect attribution of the driver of observed genetic structure. Second, we evaluated the power of causal modelling with partial Mantel tests on resistance gradients to correctly identify the explanatory model and reject incorrect alternative models. Third, we evaluated how rapidly after the landscape genetic process is initiated that we are able to reliably detect the effect of the correct model and reject the incorrect models. Our analyses suggest that simple correlational analyses between genetic data and proposed explanatory models produce strong spurious correlations, which lead to incorrect inferences. We found that causal modelling was extremely effective at rejecting incorrect explanations and correctly identifying the true causal process. We propose a generalized framework for landscape genetics based on analysis of the spatial genetic relationships among individual organisms relative to alternative hypotheses that define functional relationships between landscape features and spatial population processes.

Abstract:The predominant analytical approach to associate landscape patterns with gene flow processes is based on the association of cost distances with genetic distances between individuals. Mantel and partial Mantel tests have been the dominant statistical tools used to correlate cost distances and genetic distances in landscape genetics. However, the inherent high correlation among alternative resistance models results in a high risk of spurious correlations using simple Mantel tests. Several refinements, including causal modeling, have been developed to reduce the risk of affirming spurious correlations and to assist model selection. However, the evaluation of these approaches has been incomplete in several respects. To demonstrate the general reliability of the causal modeling approach with Mantel tests, it must be shown to be able to correctly identify a wide range of landscape resistance models as the correct drivers relative to alternative hypotheses. The objectives of this study were to (1) evaluate the effectiveness of the originally published causal modeling framework to support the correct model and reject alternative hypotheses of isolation by distance and isolation by barriers and to (2) evaluate the effectiveness of causal modeling involving direct competition of all hypotheses to support the correct model and reject all alternative landscape resistance models. We found that partial Mantel OPEN ACCESSDiversity 2013, 5 52 tests have very low Type II error rates, but elevated Type I error rates. This leads to frequent identification of support for spurious correlations between alternative resistance hypotheses and genetic distance, independent of the true resistance model. The frequency in which this occurs is directly related to the degree of correlation between true and alternative resistance models. We propose an improvement based on the relative support of the causal modeling diagnostic tests.

Spatially explicit simulation of gene flow in complex landscapes is essential to explain observed population responses and provide a foundation for landscape genetics. To address this need, we wrote a spatially explicit, individual-based population genetics model (cdpop). The model implements individual-based population modelling with Mendelian inheritance and k-allele mutation on a resistant landscape. The model simulates changes in population and genotypes through time as functions of individual based movement, reproduction, mortality and dispersal on a continuous cost surface. This model will be a valuable tool for the study of landscape genetics by increasing our understanding about the effects of life history, vagility and differential models of landscape resistance on the genetic structure of populations in complex landscapes.