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What doesn't kill them makes them stronger: an association between elongation factor 1-α overdominance in the sea star Pisaster ochraceus and "sea star wasting disease".

ABSTRACT: In recent years, a massive mortality event has killed millions of sea stars, of many different species, along the Pacific coast of North America. This disease event, known as 'sea star wasting disease' (SSWD), is linked to viral infection. In one affected sea star (Pisaster ochraceus), previous work had identified that the elongation factor 1-α locus (EF1A) harbored an intronic insertion allele that is lethal when homozygous yet appears to be maintained at moderate frequency in populations through increased fitness for heterozygotes. The environmental conditions supporting this increased fitness are unknown, but overdominance is often associated with disease. Here, we evaluate populations of P. ochraceus to identify the relationship between SSWD and EF1A genotype. Our data suggest that there may be significantly decreased occurrence of SSWD in individuals that are heterozygous at this locus. These results suggest further studies are warranted to understand the functional relationship between diversity at EF1A and survival in P. ochraceus.

SUBMITTER: Wares JP

PROVIDER: S-EPMC4824914 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Disease emergence occurs within the context of ecological communities, and disease driven declines in host populations can lead to complex direct and indirect ecological effects. Varying effects of a single disease among multiple susceptible hosts could benefit relatively resistant species. Beginning in 2013, an outbreak of sea star wasting disease (SSWD) led to population declines of many sea star species along the west coast of North America. Through field surveys and laboratory experiments, we investigated how and why the relative abundances of two co-occurring sea star species, Evasterias troschelii and Pisaster ochraceus, shifted during the ongoing wasting epidemic in Burrard Inlet, British Columbia, Canada. We hypothesized that Evasterias is competitively inferior to Pisaster but more resistant to SSWD. Thus, we predicted that SSWD-induced declines of Pisaster could mitigate the negative effects of SSWD on Evasterias, as the latter would experience competitive release. We document shifts in sea star abundance from 2008-2017: Pisaster abundance and mean size declined during the outbreak, while Evasterias abundance increased from relatively rare to numerically dominant within the intertidal. When exposed to symptomatic sea stars, Pisaster and Evasterias both showed signs of SSWD, but transmission and susceptibility was lower in Evasterias. Despite diet overlap documented in our field surveys, Evasterias was not outcompeted by Pisaster in laboratory trails conducted with the relatively small Pisaster available after the outbreak. Interference competition with larger Pisaster, or prey exploitation by Pisaster during the summer when Evasterias is primarily subtidal, may explain the rarity of Evasterias prior to Pisaster declines. Our results suggest that indirect effects mediated by competition can mask some of the direct effects of disease outbreaks, and the combination of direct and indirect effects will determine the restructuring of a community after disturbance.

Project description:Sea star wasting disease (SSWD) first appeared in Oregon in April 2014, and by June had spread to most of the coast. Although delayed compared to areas to the north and south, SSWD was initially most intense in north and central Oregon and spread southward. Up to 90% of individuals showed signs of disease from June-August 2014. In rocky intertidal habitats, populations of the dominant sea star Pisaster ochraceus were rapidly depleted, with magnitudes of decline in density among sites ranging from -2x to -9x (59 to 84%) and of biomass from -2.6x to -15.8x (60 to 90%) by September 2014. The frequency of symptomatic individuals declined over winter and persisted at a low rate through the spring and summer 2015 (~5-15%, at most sites) and into fall 2015. Disease expression included six symptoms: initially with twisting arms, then deflation and/or lesions, lost arms, losing grip on substrate, and final disintegration. SSWD was disproportionally higher in orange individuals, and higher in tidepools. Although historically P. ochraceus recruitment has been low, from fall 2014 to spring 2015 an unprecedented surge of sea star recruitment occurred at all sites, ranging from ~7x to 300x greater than in 2014. The loss of adult and juvenile individuals in 2014 led to a dramatic decline in predation rate on mussels compared to the previous two decades. A proximate cause of wasting was likely the "Sea Star associated Densovirus" (SSaDV), but the ultimate factors triggering the epidemic, if any, remain unclear. Although warm temperature has been proposed as a possible trigger, SSWD in Oregon populations increased with cool temperatures. Since P. ochraceus is a keystone predator that can strongly influence the biodiversity and community structure of the intertidal community, major community-level responses to the disease are expected. However, predicting the specific impacts and time course of change across west coast meta-communities is difficult, suggesting the need for detailed coast-wide investigation of the effects of this outbreak.

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What doesn't kill them makes them stronger: an association between elongation factor 1-α overdominance in the sea star Pisaster ochraceus and "sea star wasting disease".

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