Discussion
The recent outbreaks of SSWS at multiple coastal sites caused severe population declines in several sea star species. Mitigation techniques for addressing outbreaks when causative agent(s) is unknown should run parallel with studies attempting to determine the cause (Groner et al., 2016).  With the rising sea water temperatures resulting in the higher prevalence of marine diseases (Harvell et al., 2002; Tracy, Pielmeier, Yoshioka, Heron, & Harvell, 2019), we are likely to see similar scenarios of mass mortality outbreaks impacting marine species more frequently and having little time to address management or conservation plans. Assessing the potential for natural population resilience is a critical step in predicting the long-term fate of affected species and of the communities they in turn influence. For example, selectively rearing disease-resistant oysters in hatcheries has been a useful tool in avoiding disease outbreaks that are decimating wild populations (Agnew et al., 2020; Dégremont, Garcia, & Allen, 2015). While many marine species are not amenable for selective breeding, examining genomic variation in natural populations can address whether these species have the genetic makeup for adaptation to marine diseases on their own. 
In this study, we took advantage of the co-occurrence of wasting and apparently normal individuals of P. ochraceus in central Oregon to scan for genomic regions that potentially predict individual SSWS status. After genotyping nearly 72,000 SNP loci across 133 individuals, we found no strong patterns of differentiation between wasting and apparently normal individuals. Loci with elevated Fst were not clearly concentrated as peaks in any genomic region, and no single locus showed statistically significant level of allele frequency differences. Using a multivariate approach as a complement to the locus-specific Fst analyses, 18 SNP loci stood out as contributing to genomic differentiation between the two groups of individuals based on disease status. Overall, we argue that a genetic basis for SSWS resilience in P. ochraceus is likely weak, but we identified a list of genomic regions and functional candidates that may serve as basis for studies of gene expression, physiology, or comparative genomics during future SSWS outbreaks.
While the proximate cause(s) of SSWS at the individual level are still unknown, recent experimental studies are consistent with a pathogen agent. For example, individuals that were wasting in the laboratory showed physiological and gene expression response suggestive of innate immunity, cytokine-like systems, and tissue remodeling (Fuess et al., 2015; Gudenkauf & Hewson, 2015; Ruiz‐Ramos et al., 2020). Our findings showed no evidence for strong genetic component to SSWS tolerance or resistance, but the weakly-associated loci we identified may have small but cumulative effects, which is expected for a polygenic trait. This trait may hence require much higher powered studies for detecting associated loci with more precision (Gagnaire & Gaggiotti, 2016).