Little evidence for genetic variation associated with susceptibility to sea star wasting syndrome in the keystone species Pisaster ochraceus.

The keystone species Pisaster ochraceus suffered mass mortalities along the northeast Pacific Ocean from Sea Star Wasting Syndrome (SSWS) outbreaks in 2013-2016. SSWS causation remains of debate, leading to concerns as to whether outbreaks will continue to impact this species. Considering the apparent link between ocean temperature and SSWS, the future of this species and intertidal communities remains uncertain. Surveys of co-occurring apparently normal and wasting P. ochraceus along the central Oregon coast in 2016 allowed us to address whether variation in disease status showed genetic variation that may be associated with differences in susceptibility to SSWS. We performed restriction site-associated DNA sequencing (2bRAD-seq) to genotype ~72,000 single nucleotide polymorphism (SNP) loci across apparently normal and wasting sea stars. Locus-specific analyses of differentiation (F ) between disease-status groups revealed no signal of genetic differences separating the two groups. Using a multivariate approach, we observed weak separation between the groups, but identified 18 SNP loci showing highest discriminatory power between the groups and scanned the genome annotation for linked genes. A total of 34 protein-coding genes were found to be located within 15 kb (measured by linkage disequilibrium decay) of at least one of the 18 SNPs, and 30 of these genes had homologies to annotated protein databases. Our results suggest that the likelihood of developing SSWS symptoms does not have a strong genetic basis. The few genomic regions highlighted had only modest levels of differentiation, but the genes associated with these regions may form the basis for functional studies aiming to understand disease progression.