Spatially-explicit estimation of Wright's neighborhood size in continuous populations

Effective population size (Ne) is an important parameter in conservation genetics because it quantifies a population’s capacity to resist loss of genetic diversity due to inbreeding and drift. The classical approach to estimate Ne from genetic data involves grouping sampled individuals into discretely defined subpopulations assumed to be panmictic. Importantly, this assumption does not capture the continuous nature of populations genetically isolated by distance. Alternative approaches based on Wright’s genetic neighborhood concept quantify the local number of breeding individuals (NS) in a continuous population (as opposed to the global Ne). However, they do not reflect the potential for NS to vary spatially nor do they account for the resistance of a heterogeneous landscape to gene flow (isolation by resistance). Here, we describe an application of Wright’s neighborhood concept that provides spatially-explicit estimates of local NS from genetic data in continuous populations isolated by distance or resistance. We delineated local neighborhoods surrounding each sampled individual based on sigma (), a measure of the local extent of breeding. When was known, the linkage disequilibrium method applied to local neighborhoods produced unbiased estimates of NS that were highly variable across the landscape. NS near the periphery or areas surrounded by high resistance was as much as an order of magnitude lower compared to the center, raising the potential for a spatial component to extinction vortex dynamics in continuous populations. When is not known, it may be estimated from genetic data, but two methods we evaluated identified analysis extents that produced considerable bias or error in the estimate of NS. When is known or accurately estimated, and the assumptions of Wright’s neighborhood are met, the method we describe provides spatially explicit information regarding short-term genetic processes that may inform conservation genetic analyses and management

Re-evaluating causal modeling with mantel tests in landscape genetics

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 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

Multiple major increases and decreases in mitochondrial substitution rates in the plant family Geraniaceae

Background: Rates of synonymous nucleotide substitutions are, in general, exceptionally low in plant mitochondrial genomes, several times lower than in chloroplast genomes, 10-20 times lower than in plant nuclear genomes, and 50-100 times lower than in many animal mitochondrial genomes. Several cases of moderate variation in mitochondrial substitution rates have been reported in plants, but these mostly involve correlated changes in chloroplast and/or nuclear substitution rates and are therefore thought to reflect whole-organism forces rather than ones impinging directly on the mitochondrial mutation rate. Only a single case of extensive, mitochondrial-specific rate changes has been described, in the angiosperm genus Plantago. Results: We explored a second potential case of highly accelerated mitochondrial sequence evolution in plants. This case was first suggested by relatively poor hybridization of mitochondrial gene probes to DNA of Pelargonium hortorum (the common geranium). We found that all eight mitochondrial genes sequenced from P. hortorum are exceptionally divergent, whereas chloroplast and nuclear divergence is unexceptional in P. hortorum. Two mitochondrial genes were sequenced from a broad range of taxa of variable relatedness to P. hortorum, and absolute rates of mitochondrial synonymous substitutions were calculated on each branch of a phylogenetic tree of these taxa. We infer one major, similar to 10-fold increase in the mitochondrial synonymous substitution rate at the base of the Pelargonium family Geraniaceae, and a subsequent similar to 10-fold rate increase early in the evolution of Pelargonium. We also infer several moderate to major rate decreases following these initial rate increases, such that the mitochondrial substitution rate has returned to normally low levels in many members of the Geraniaceae. Finally, we find unusually little RNA editing of Geraniaceae mitochondrial genes, suggesting high levels of retroprocessing in their history. Conclusion: The existence of major, mitochondrial-specific changes in rates of synonymous substitutions in the Geraniaceae implies major and reversible underlying changes in the mitochondrial mutation rate in this family. Together with the recent report of a similar pattern of rate heterogeneity in Plantago, these findings indicate that the mitochondrial mutation rate is a more plastic character in plants than previously realized. Many molecular factors could be responsible for these dramatic changes in the mitochondrial mutation rate, including nuclear gene mutations affecting the fidelity and efficacy of mitochondrial DNA replication and/or repair and consistent with the lack of RNA editing - exceptionally high levels of mutagenic retroprocessing. That the mitochondrial mutation rate has returned to normally low levels in many Geraniaceae raises the possibility that, akin to the ephemerality of mutator strains in bacteria, selection favors a low mutation rate in plant mitochondria

Predicting Landscape-Genetic Consequences of Habitat Loss, Fragmentation and Mobility for Multiple Species of Woodland Birds

Inference concerning the impact of habitat fragmentation on dispersal and gene flow is a key theme in landscape genetics. Recently, the ability of established approaches to identify reliably the differential effects of landscape structure (e.g. land-cover composition, remnant vegetation configuration and extent) on the mobility of organisms has been questioned. More explicit methods of predicting and testing for such effects must move beyond post hoc explanations for single landscapes and species. Here, we document a process for making a priori predictions, using existing spatial and ecological data and expert opinion, of the effects of landscape structure on genetic structure of multiple species across replicated landscape blocks. We compare the results of two common methods for estimating the influence of landscape structure on effective distance: least-cost path analysis and isolation-by-resistance. We present a series of alternative models of genetic connectivity in the study area, represented by different landscape resistance surfaces for calculating effective distance, and identify appropriate null models. The process is applied to ten species of sympatric woodland-dependant birds. For each species, we rank a priori the expectation of fit of genetic response to the models according to the expected response of birds to loss of structural connectivity and landscape-scale tree-cover. These rankings (our hypotheses) are presented for testing with empirical genetic data in a subsequent contribution. We propose that this replicated landscape, multi-species approach offers a robust method for identifying the likely effects of landscape fragmentation on dispersal

Adhesion assays on collagen I using were performed with no growth factor (open bars), 10 nM EGF (closed bars) or 10 nM HRG-α (hatched bars)

<p><b>Copyright information:</b></p><p>Taken from "Epidermal growth factor mediates detachment from and invasion through collagen I and Matrigel in Capan-1 pancreatic cancer cells"</p><p>BMC Gastroenterology 2005;5():12-12.</p><p>Published online 31 Mar 2005</p><p>PMCID:PMC1079814.</p><p>Copyright © 2005 Shirk and Kuver; licensee BioMed Central Ltd.</p> Shown are the results of three separate experiments, each performed in triplicate. * p < 0.001

Cells were labeled and invasion through chambers performed in the absence or presence of 10 nM EGF

<p><b>Copyright information:</b></p><p>Taken from "Epidermal growth factor mediates detachment from and invasion through collagen I and Matrigel in Capan-1 pancreatic cancer cells"</p><p>BMC Gastroenterology 2005;5():12-12.</p><p>Published online 31 Mar 2005</p><p>PMCID:PMC1079814.</p><p>Copyright © 2005 Shirk and Kuver; licensee BioMed Central Ltd.</p> Shown are the results of one experiment performed in triplicate wells, which was repeated twice with similar results

Cells were cultured on Transwell inserts, and confocal immunofluorescence microscopy performed following incubation with TRITC-conjugated phalloidin, in the absence (A) or presence (B) of 10 nM EGF

<p><b>Copyright information:</b></p><p>Taken from "Epidermal growth factor mediates detachment from and invasion through collagen I and Matrigel in Capan-1 pancreatic cancer cells"</p><p>BMC Gastroenterology 2005;5():12-12.</p><p>Published online 31 Mar 2005</p><p>PMCID:PMC1079814.</p><p>Copyright © 2005 Shirk and Kuver; licensee BioMed Central Ltd.</p> Arrow shows focal area of actin staining consistent with a focal adhesion complex

Cells were cultured on invasion chambers coated with Matrigel, and invasion measured following treatment with no growth factor, 10 nM EGF, or 10 nM HRG-α

<p><b>Copyright information:</b></p><p>Taken from "Epidermal growth factor mediates detachment from and invasion through collagen I and Matrigel in Capan-1 pancreatic cancer cells"</p><p>BMC Gastroenterology 2005;5():12-12.</p><p>Published online 31 Mar 2005</p><p>PMCID:PMC1079814.</p><p>Copyright © 2005 Shirk and Kuver; licensee BioMed Central Ltd.</p> Shown are the results of 3 experiments, each performed in triplicate wells. *p < 0.05 between the no growth factor group and the EGF treatment group for each cell type

Cells were cultured on Transwell inserts, and confocal immunofluorescence microscopy performed following incubation with primary antibodies against EGF-R (A), αintegrin (B) and βintegrin (C)

<p><b>Copyright information:</b></p><p>Taken from "Epidermal growth factor mediates detachment from and invasion through collagen I and Matrigel in Capan-1 pancreatic cancer cells"</p><p>BMC Gastroenterology 2005;5():12-12.</p><p>Published online 31 Mar 2005</p><p>PMCID:PMC1079814.</p><p>Copyright © 2005 Shirk and Kuver; licensee BioMed Central Ltd.</p> Negative controls with primary antibody omitted did not show a detectable signal