Saltwater- and freshwater environments have opposing physiological challenges, yet, there are fish species that are able to enter both habitats during short time-spans, and as individuals they must therefore adjust quickly to osmoregulatory contrasts. In this study, we conducted an experiment to test for plastic responses to abrupt sainity changes in two poplulations of threespine stickleback, Gasterosteus aculeatus, representing two ecotypes (freshwater and ancestral saltwater). We exposed both ecotypes to abrupt native (control treatment) and non-native salinities (0 and 30‰) and sampled gill-tissue for transcriptomic analyses after six hours exposure. To investigate genomic responses to salinity, we analysed four different comparisons; one for each ecotype (in their control and exposure salinity; 1 and 2), one between ecotypes in their control salinity (3), and the fourth comparison included all transcripts identified in (3) that did not show any expressional changes within ecotype in either the control or the exposed salinity (4). Abrupt salinity transfer affected the expression of 10 and 1530 transcripts for the saltwater and freshwater ecotype, respectively, and 1314 were differentially expressed between the controls, including 502 that were not affected by salinity within ecotype (fixed expression). In total, these results indicate that factors other than genomic expressional plasticity are important for osmoregulation in stickleback, due to the need for opposite physiological pathways to survive the abrupt change in salinity.

Pathogens may elicit a high selective pressure on hosts and can alter genetic diversity over short evolutionary timescales. Intraspecific variation in immune response can be observed as variable survivability from specific infections. The great gerbil (Rhombomys opimus) is a rodent plague host with a heterogenic but highly resistant phenotype. Here, we investigate if the most plague-resistant phenotypes are linked to genomic differences between survivors and susceptible individuals by exposure of wild-caught great gerbils from Northwest China to plague (Yersinia pestis). Whole genome sequencing of ten survivors and ten moribund individuals revealed a low genome-wide mean divergence, except for a subset of genomic regions that showed elevated differentiation. Gene ontology (GO) analysis of candidate genes within regions of increased differentiation, demonstrated enrichment of pathways involved in transcription and translation and their regulation), as well as genes directly involved in immune functions, cellular metabolism and the regulation of apoptosis. Differential RNA expression analysis revealed that the early activated great gerbil immune response to plague consisted of classical components of the innate immune system. Our approach combining challenge experiments with transcriptomics and population level sequencing, provides new insight into the genetic background of plague-resistance and confirms its complex nature, most likely involving multiple genes and pathways of both the immune system and regulation of basic cellular functions.