| Summary: | The New Zealand sea lion (NZSL) is the rarest sea lion in the world and exists in relative isolation, primarily in New Zealand’s sub-Antarctic islands. Once widespread throughout New Zealand, the species suffered a population bottleneck through subsistence and exploitative hunting. Only 8600 – 11300 individuals remain and pup production has declined by 40% over the last decade. In addition, the species is unusually susceptible to disease and has suffered three seasons of very high pup mortality in recent years (1997 – 2003). As such, it is of high conservation concern. Here we have applied population genetics and molecular ecological methods to address how genetic factors may be impacting the susceptibility of the NZSL to disease. First, since the level of variation at neutral genomic loci is expected to be a reasonably good predictor of overall genomic variation, we dissected the level of variation at a large panel of microsatellite loci, and established that while heterozygosity is maintained, allelic diversity is depauperate. We have also provided genetic evidence of an historical population-size bottleneck, and indicated that the population departs from random mating and panmixia, as expected under Hardy-Weinberg equilibrium. Next, because of the difficulties associated with the anonymity of microsatellite loci in species for which no genome sequence exists, we created a predicted physical map of the pinniped genome using microsatellites, based on demonstrated synteny between species of the Carnivora. We optimised and then utilised a panel of 21 microsatellite loci to show that overall genetic variation in NZSL pups is associated with death by bacterial infection, and that the panel of microsatellites used here is reflective of genome-wide variation, justifying its utility in the context of HFCs. However, the level of variation at neutral genomic loci is not necessarily correlated with variation elsewhere in the genome; therefore it was important to investigate variation at genes with known function in disease resistance or susceptibility. We have illustrated that the gene SLC11A1 (previously NRAMP1) has conserved structural features in the NZSL reflective of its role in macrophage activation; however we lacked the statistical power to associate variations in this gene with disease in this study, despite promising trends. We then demonstrated a high level of variation at one gene of the major histocompatibility complex (MHC), in spite of low allelic diversity at microsatellite loci. The NZSL has been subject to recurrent epizootic events in recent years, attributable to two different bacterial pathogens. We suggest that, as a consequence of recurrent selection pressure exerted by diverse pathogens and multiple epizootic events, balancing selection may be operating at this locus in order to maintain MHC diversity, which is generally vital for an adequate immune response. In addition, certain haplotypes of this gene associated strongly with survival; however these results should be viewed as tentative. In summary, we have presented a thorough assessment of genome-wide variation in the NZSL and conclude that diversity is generally low; however selection appears to be maintaining variation at genes involved in the immune response, and this work provides intriguing preliminary data for further study. This research serves to elucidate overall levels of genetic variation in this endemic, threatened species, and aids in the understanding of the genetic mechanisms of resistance to disease epizootics, which is crucial for their conservation management and population recovery. This work has the capacity to be applied to many species of conservation concern both in New Zealand and globally.
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