Genetic variation associated with lower 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. Causation of SSWS is still debated, 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. We surveyed populations of sea stars along the Oregon coast in 2016, two years after the epidemic began. Cohabitation of asymptomatic and symptomatic individuals allowed us to ask whether lower susceptibility in asymptomatic individuals differed genetically. We performed restriction site-associated DNA sequencing (2bRAD-seq) to genotype thousands of single nucleotide polymorphism (SNP) loci. By comparing allele frequencies between symptomatic and asymptomatic individuals, we detected three loci that may be under selection. A multivariate analysis showed a clear separation between groups based on disease status in two of the three geographic regions, along with several regions across the genome having small statistical contributions to this separation. A draft annotation of protein-coding regions allowed us to identify 120 predicted genes that are linked to these markers and are putatively associated with lower susceptibility. Our results suggest that some variation in disease severity can be attributed to genetic variation. However, differences in phenotype have a highly polygenic nature with no single or few genomic regions having strong predictive effects. The genes associated with these regions may form the basis for functional studies aiming to understand disease progression in infected individuals.

Virome Variation during Sea Star Wasting Disease Progression in Pisaster ochraceus (Asteroidea, Echinodermata)

Sea star wasting disease (SSWD) is a condition that has affected asteroids for over 120 years, yet mechanistic understanding of this wasting etiology remains elusive. We investigated temporal virome variation in two Pisaster ochraceus specimens that wasted in the absence of external stimuli and two specimens that did not experience SSWD for the duration of our study, and compared viromes of wasting lesion margin tissues to both artificial scar margins and grossly normal tissues over time. Global assembly of all SSWD-affected tissue libraries resulted in 24 viral genome fragments represented in >1 library. Genome fragments mostly matched densoviruses and picornaviruses with fewer matching nodaviruses, and a sobemovirus. Picornavirus-like and densovirus-like genome fragments were most similar to viral genomes recovered in metagenomic study of other marine invertebrates. Read recruitment revealed only two picornavirus-like genome fragments that recruited from only SSWD-affected specimens, but neither was unique to wasting lesions. Wasting lesion margin reads recruited to a greater number of viral genotypes (i.e., richness) than did either scar tissue and grossly normal tissue reads. Taken together, these data suggest that no single viral genome fragment was associated with SSWD. Rather, wasting lesion margins may generally support viral proliferation.

Virome Temporal Variation During Sea Star Wasting Disease Progression in Pisaster ochraceus (Asteroidea, Echinodermata)

Sea star wasting disease (SSWD) is a condition that has affected asteroids for over 120 years, yet mechanistic understanding of wasting etiology remains elusive. We investigated temporal virome variation in two Pisaster ochraceus specimens that wasted in the absence of external stimuli and two specimens that did not experience SSWD for the duration of our study, and compared viromes of wasting lesion margin tissues to both artificial scar margins and grossly normal tissues over time. Global assembly of all SSWD-affected tissue libraries resulted in 45 viral genome fragments represented in >1 library. Genome fragments mostly matched densoviruses and picornaviruses with fewer matching nodaviruses, narnaviruses and sobemoviruses. Picornavirus-like and densovirus-like genome fragments were most similar to viral genomes recovered in metagenomic study of other marine invertebrates. Read recruitment revealed only 2 picornavirus-like genome fragments that recruited from only SSWD-affected specimens, but neither was unique to wasting lesions. Wasting lesion margin reads recruited to a greater number of viral genotypes (i.e. richness) than did either scar tissue and grossly normal tissue reads. Taken together, these data suggest that no single viral genome fragment was associated with SSWD. Rather, wasting lesion margins may generally support viral proliferation.

Testing ecological release as a compensating mechanism for mass mortality in a keystone predator

Top predator decline has been ubiquitous across systems over the past decades and centuries, and predicting changes in resultant community dynamics is a major challenge for ecologists and managers. Ecological release predicts that loss of a limiting factor, such as a dominant competitor or predator, can release a species from control, thus allowing increases in its size, density, and/or distribution. The 2014 sea star wasting syndrome (SSWS) outbreak decimated populations of the keystone predator Pisaster ochraceus along the Oregon coast, USA. This event provided an opportunity to test the predictions of ecological release across a broad spatial scale and determine the role of competitive dynamics in top predator recovery. We hypothesized that after P. ochraceus loss, populations of the subordinate sea star Leptasterias sp. would grow larger, more abundant, and move downshore. We based these predictions on prior research in Washington State showing that Leptasterias sp. competed with P. ochraceus for food. Further, we predicted that ecological release of Leptasterias sp. could provide a bottleneck to P. ochraceus recovery. Using field surveys, we found no clear change in density or distribution in Leptasterias sp. populations post-SSWS, and decreases in body size. In a field experiment, we found no evidence of competition between similar-sized Leptasterias sp. and P. ochraceus. Thus, the mechanisms underlying our predictions were not in effect along the Oregon coast, which we attribute to differences in habitat overlap and food availability between the 2 regions. Our results suggest that response to the loss of a dominant competitor can be unpredictable even when based in theory and previous research.