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An overdominant mutation in the elongation factor 1-alpha (EF1A) gene in the sea star Pisaster ochraceus has shown itself to mediate tolerance to "sea star wasting disease", a pandemic that has significantly reduced sea star populations on the Pacific coast of North America. Here we use RNA sequencing of healthy individuals to identify differences in constitutive expression of gene regions that may help explain this tolerance phenotype. Our results show that individuals carrying this single mutation have lower expression at a large contingent of gene regions, and it appears likely that the EF1A locus itself is similarly affected, with a 2-fold reduction in expression of some EF1A transcripts. Individuals without this mutation also appear to have a greater cellular response to temperature stress, which has been implicated in the outbreak of sea star wasting disease. Given the ecological significance of P. ochraceus and the key role of EF1A in cellular composition and maintenance, these results may be useful in predicting the evolutionary and demographic future for Pacific intertidal communities.
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Supplemental Table S1
Supplemental Table S1. Library name, EF1A genotype, RNA quality (RIN), SRA Accession, library size, righting response (seconds; standard deviation in parentheses), and percentage of reads mapped to the Trinity assembly. Libraries for Po1 and Po2 (both temperature treatments) contributed to the reduced-input assembly. All sequence data are archived at NCBI in BioProject PRJNA357374.
Supplement S2. Fold change, log CPM, P-value, and FDR for Trinity fragments generated for this analysis, excluding individual Po5. Where available, BLAST identifiers are given; only BLAST hits with an e-value of < 10^-6 are included.