Aim Present Amazonian diversity patterns can result from many different mechanisms and, consequently, the factors contributing to divergence across regions and/or taxa may differ. Nevertheless, the river‐barrier hypothesis is still widely invoked as a causal process in divergence of Amazonian species. Here we use model‐based phylogeographic analyses to test the extent to which major Amazonian rivers act similarly as barriers across time and space in two broadly distributed Amazonian taxa. Local Amazon rain forest. Taxon The lizard Gonatodes humeralis (Sphaerodactylidae) and the tree frog Dendropsophus leucophyllatus (Hylidae). Methods We obtained RADseq data for samples distributed across main river barriers, representing main Areas of Endemism previously proposed for the region. We conduct model‐based phylogeographic and genetic differentiation analyses across each population pair. Results Measures of genetic differentiation (based on FST calculated from genomic data) show that all rivers are associated with significant genetic differentiation. Parameters estimated under investigated divergence models showed that divergence times for populations separated by each of the 11 bordering rivers were all fairly recent. The degree of differentiation consistently varied between taxa and among rivers, which is not an artifact of any corresponding difference in the genetic diversities of the respective taxa, or to amounts of migration based on analyses of the site‐frequency spectrum. Main conclusions Taken together, our results support a dispersal (rather than vicariance) history, without strong evidence of congruence between these species and rivers. However, once a species crossed a river, populations separated by each and every river have remained isolated—in this sense, rivers act similarly as barriers to any further gene flow. This result suggests differing degrees of persistence and gives rise to the seeming contradiction that the divergence process indeed varies across time, space and species, even though major Amazonian rivers have acted as secondary barriers to gene flow in the focal taxa.

Closely related populations often differ in resistance to a given parasite, as measured by infection success or failure. Yet, the immunological mechanisms of these evolved differences are rarely specified. Does resistance evolve via changes to the host's ability to recognize that an infection exists, actuate an effective immune response, or attenuate that response? We tested whether each of these phases of the host response contributed to threespine sticklebacks’ recently evolved resistance to their tapeworm Schistocephalus solidus. Although marine stickleback and some susceptible lake fish permit fast‐growing tapeworms, other lake populations are resistant and suppress tapeworm growth via a fibrosis response. We subjected lab‐raised fish from three populations (susceptible marine “ancestors,” a susceptible lake population, and a resistant lake population) to a novel immune challenge using an injection of (1) a saline control, (2) alum, a generalized pro‐inflammatory adjuvant that causes fibrosis, (3) a tapeworm protein extract, or (4) a combination of alum and tapeworm protein. With enough time, all three populations generated a robust fibrosis response to the alum treatments. Yet, only the resistant population exhibited a fibrosis response to the tapeworm protein alone. Thus, these populations differed in their ability to respond to the tapeworm protein but shared an intact fibrosis pathway. The resistant population also initiated fibrosis faster in response to alum, and was able to attenuate fibrosis, unlike the susceptible populations’ slow but longer lasting response to alum. As fibrosis has pathological side effects that reduce fecundity, the faster recovery by the resistant population may reflect an adaptation to mitigate the costs of immunity. Broadly, our results confirm that parasite detection and immune initiation, activation speed, and immune attenuation simultaneously contribute to the evolution of parasite resistance and adaptations to infection in natural populations.