Understanding the mechanisms involved in pathogen adaptation to quantitative resistance in plants has a key role to play in establishing durable strategies for resistance deployment, especially in perennial crops. The erosion of quantitative resistance has been recently suspected in Cuba and the Dominican Republic for a major fungal pathogen of such a crop Pseudocercospora fijiensis, causing black leaf streak disease on banana. This study set out to test whether such erosion has resulted from an adaptation of P. fijiensis populations, and to determine whether or not the adaptation is local. Almost 600 P. fijiensis isolates from Cuba and the Dominican Republic were sampled using a paired-population sampling design on resistant and susceptible banana varieties. A low genetic structure of the P. fijiensis populations was detected in each country using 16 microsatellite markers. Cross-inoculation experiments using isolates from susceptible and resistant cultivars were carried out, measuring a quantitative trait (the diseased leaf area) related to pathogen fitness on three varieties. A further analysis based on those data suggested the existence of a local pattern of adaptation to resistant cultivars in both of the study countries, due to the existence of specific (or genotype by genotype) host-pathogen interactions. However, neither cost nor benefit effects for adapted populations were found on the widely used "Cavendish" banana group. These results highlight the need to study specific host-pathogen interactions and pathogen adaptation on a wide range of quantitative resistance phenotypes in banana, in order to develop durable strategies for resistance deployment. © 2019 The Authors. Evolutionary Applications published by John Wiley & Sons Ltd.In bacteria, evolution of resistance to one antibiotic is frequently associated with increased resistance (cross-resistance) or increased susceptibility (collateral sensitivity) to other antibiotics. Cross-resistance and collateral sensitivity are typically evaluated at the minimum inhibitory concentration (MIC). However, these susceptibility changes are not well characterized with respect to the mutant prevention concentration (MPC), the antibiotic concentration that prevents a single-step mutation from occurring. We measured the MIC and the MPC for Staphylococcus epidermidis and 14 single-drug resistant strains against seven antibiotics. https://www.selleckchem.com/products/AZD1152-HQPA.html We found that the MIC and the MPC were positively correlated but that this correlation weakened if cross-resistance did not evolve. If any type of resistance did evolve, the range of concentrations between the MIC and the MPC tended to shift right and widen. Similar patterns of cross-resistance and collateral sensitivity were observed at the MIC and MPC levels, though more symmetry was observed at the MIC level. Whole-genome sequencing revealed mutations in both known-target and nontarget genes. Moving forward, examining both the MIC and the MPC may lead to better predictions of evolutionary trajectories in antibiotic-resistant bacteria. © 2019 The Authors. Evolutionary Applications published by John Wiley & Sons Ltd.An understanding of how genetic variability is distributed in space is fundamental for the conservation and maintenance of diversity in spatially fragmented and vulnerable populations. While fragmentation can occur from natural barriers, it can also be exacerbated by anthropogenic activities such as hydroelectric power plant development. Whatever the source, fragmentation can have significant ecological effects, including disruptions of migratory processes and gene flow among populations. In Chile, the Biobío River basin exhibits a high degree of habitat fragmentation due to the numerous hydroelectric power plants in operation, the number of which is expected to increase following new renewable energy use strategies. Here, we assessed the effects of different kinds of barriers on the genetic structure of the endemic freshwater fish Percilia irwini, knowledge that is critically needed to inform conservation strategies in light of current and anticipated further fragmentation initiatives in the system. We identified eight genetic units throughout the entire Biobío system with high effective sizes. A reduced effective size estimate was, however, observed in a single population located between two impassable barriers. Both natural waterfalls and human-made dams were important drivers of population differentiation in this system; however, dams affect genetic diversity differentially depending on their mode of operation. Evidence of population extirpation was found in two river stretches limited by upstream and downstream dams. Significant gene flow in both directions was found among populations not separated by natural or anthropogenic barriers. Our results suggest a significant vulnerability of P. irwini populations to future dam development and demonstrate the importance of studying basin-wide data sets with genetic metrics to understand the strength and direction of anthropogenic impacts on fish populations. © 2019 The Authors. Evolutionary Applications published by John Wiley & Sons Ltd.The ultimate causes of correlated evolution among sites in a genome remain difficult to tease apart. To address this problem directly, we performed a high-throughput search for correlated evolution among sites associated with resistance to a fluoroquinolone antibiotic using whole-genome data from clinical strains of Pseudomonas aeruginosa, before validating our computational predictions experimentally. We show that for at least two sites, this correlation is underlain by epistasis. Our analysis also revealed eight additional pairs of synonymous substitutions displaying correlated evolution underlain by physical linkage, rather than selection associated with antibiotic resistance. Our results provide direct evidence that both epistasis and physical linkage among sites can drive the correlated evolution identified by high-throughput computational tools. In other words, the observation of correlated evolution is not by itself sufficient evidence to guarantee that the sites in question are epistatic; such a claim requires additional evidence, ideally coming from direct estimates of epistasis, based on experimental evidence.