Search for: All records

Abstract Understanding the forces that drive genotypic and phenotypic change in wild populations is a central goal of evolutionary biology. We examined exome variation in populations of deer mice from two of the California Channel Islands:Peromyscus maniculatus elususfrom Santa Barbara Island andP. m. santacruzaefrom Santa Cruz Island exhibit significant differences in olfactory predator recognition, activity timing, aggressive behavior, morphology, prevalence of Sin Nombre virus, and population densities. We characterized variation in protein‐coding regions using exome capture and sequencing of 25 mice from Santa Barbara Island and 22 mice from Santa Cruz Island. We identified and examined 386,256 SNPs using three complementary methods (BayeScan, pcadapt, and LFMM). We found strong differences in molecular variation between the two populations and 710 outlier SNPs in protein‐coding genes that were detected by all three methods. We identified 35 candidate genes from this outlier set that were related to differences in phenotypes between island populations. Enrichment analyses demonstrated that patterns of molecular variation were associated with biological processes related to response to chemical stimuli and regulation of immune processes. Candidate genes associated with olfaction (Gfy,Tlr2,Vmn13r2, numerous olfactory receptor genes), circadian activity (Cry1), anxiety (Brca1), immunity (Cd28,Eif2ak4, Il12a,Syne1), aggression (Cyp19a,Lama2), and body size (Bc16,Syne1) exhibited non‐synonymous mutations predicted to have moderate to large effects. Variation in olfaction‐related genes, including a stop codon in the Santa Barbara Island population, suggests loss of predator‐recognition traits at the molecular level, consistent with a lack of behavioral aversion to fox feces. These findings also suggest that divergent pathogen prevalence and population density may have influenced adaptive immunity and behavioral phenotypes, such as reduced aggression. Overall, our study indicates that ecological differences between islands are associated with signatures of selection in protein‐coding genes underlying phenotypes that promote success in those environments. 

Abstract Sin Nombre virus (SNV) is a zoonotic virus that is highly pathogenic to humans. The deer mouse,Peromyscus maniculatus, is the primary host of SNV, and SNV prevalence inP. maniculatusis an important indicator of human disease risk. Because the California Channel Islands contain permanent human settlements, receive hundreds of thousands of visitors each year, and can have extremely high densities ofP. maniculatus, surveillance for SNV in islandP. maniculatusis important for understanding the human risk of zoonotic disease. Despite the importance of surveillance on these heavily utilized islands, SNV prevalence (i.e. the proportion ofP. maniculatusthat test positive to antibodies to SNV) has not been examined in the last 13–27 years. We present data on 1,610 mice sampled for four consecutive years (2014–2017) on five of the California Channel Islands: East Anacapa, Santa Barbara, Santa Catalina, San Nicolas, and San Clemente. Despite historical data indicating SNV‐positive mice on San Clemente and Santa Catalina, we detected no SNV‐positive mice on these islands, suggesting very low prevalence or possible loss of SNV. Islands historically free of SNV (East Anacapa, Santa Barbara, and San Nicolas) remained free of SNV, suggesting that rates of pathogen introduction from other islands and/or the mainland are low. Although continued surveillance is warranted to determine whether SNV establishes on these islands, our work helps inform current human disease risk in these locations and suggests that SNV prevalence on these islands is currently very low.