No abstract

Introduced parasites threaten native host species that lack effective defenses. Such parasites increase the risk of extinction, particularly in small host populations like those on islands. If some host species are tolerant to introduced parasites, this could amplify the risk of the parasite to vulnerable host species. Recently, the introduced parasitic nest fly Philornis downsi has been implicated in the decline of Darwin's finch populations in the Galápagos Islands. In some years, 100% of finch nests fail due to P. downsi; however, other common host species nesting near Darwin's finches, such as the endemic Galápagos mockingbird (Mimus parvulus), appear to be less affected by P. downsi. We compared effects of P. downsi on mockingbirds and medium ground finches (Geospiza fortis) on Santa Cruz Island in the Galápagos. We experimentally manipulated the abundance of P. downsi in nests of mockingbirds and finches to measure the direct effect of the parasite on the reproductive success of each species of host. We also compared immunological and behavioral responses by each species of host to the fly. Although nests of the two host species had similar parasite densities, flies decreased the fitness of finches but not mockingbirds. Neither host species had a significant antibody-mediated immune response to P. downsi. Moreover, finches showed no significant increase in begging, parental provisioning, or plasma glucose levels in response to the flies. In contrast, parasitized mockingbird nestlings begged more than nonparasitized mockingbird nestlings. Greater begging was correlated with increased parental provisioning behavior, which appeared to compensate for parasite damage. The results of our study suggest that finches are negatively affected by P. downsi because they do not have such behavioral mechanisms for energy compensation. In contrast, mockingbirds are capable of compensation, making them tolerant hosts, and a possible indirect threat to Darwin's finches.

Objective: Suicide death is a highly preventable, yet growing, worldwide health crisis. To date, there has been a lack of adequately powered genomic studies of suicide, with no sizeable suicide death cohorts available for study. To address this limitation, we conducted the first comprehensive genomic analysis of suicide death, using a previously unpublished suicide cohort. Methods:The analysis sample consisted of 3,413 population-ascertained cases of European ancestry and 14,810 ancestrally matched controls. Analytical methods included principle components analysis for ancestral matching and adjusting for population stratification, linear mixed model genome-wide association testing (conditional on genetic relatedness matrix), gene and gene set enrichment testing, polygenic score analyses, as well as SNP heritability and genetic correlation estimation using LD score regression.Results: GWAS identified two genome-wide significant loci (6 SNPs, p<5x10 -8 ). Gene-based analyses implicated 19 genes on chromosomes 13, 15, 16, 17, and 19 (q<0.05). Suicide heritability was estimated h 2 =0.2463, SE = 0.0356 using summary statistics from a multivariate logistic GWAS adjusting for ancestry. Notably, suicide polygenic scores were robustly predictive of out of sample suicide death, as were polygenic scores for several other psychiatric disorders and psychological traits, particularly behavioral disinhibition and major depressive disorder. Conclusions:In this report, we identify multiple genome-wide significant loci/genes, and demonstrate robust polygenic score prediction of suicide death case-control status, adjusting for ancestry, in independent training and test sets. Additionally, we report that suicide death cases have increased genetic risk for behavioral disinhibition, major depression, autism spectrum disorder, psychosis, and alcohol use disorder relative to controls. Results demonstrate the ability of polygenic scores to robustly, and multidimensionally, predict suicide death case-control status..