Proteomic analysis of Stony Coral Tissue Loss Disease demonstrates coral-algal dysbiosis during disease progression

Stony Coral Tissue Loss Disease (SCTLD) has wreaked havoc on Caribbean reefs, yet the molecular response of corals to infection remains unclear. Prior gene expression analyses of sick corals revealed changes in immunity, cell death, and coral-algal imbalance. Now, researchers have unveiled the proteomic response of Diploria labyrinthiformis to SCTLD by comparing protein levels in healthy tissue from unaffected colonies and healthy and sick tissue from affected colonies.

These findings were juxtaposed with available metagenomic data from the same samples, which had previously uncovered significant changes in the coral microbiome due to SCTLD. The study identified 480 proteins that differed in abundance between sick and healthy tissues, but only 12 between healthy healthy and healthy tissues. Pathway-level evaluation suggests that immunity is suppressed in otherwise healthy tissue, implying that the host's molecular reactions may precede observable disease.

Sick tissue exhibited signs of healing wounds alongside a decrease in proteins crucial for symbiotic relationships and an uptick in proteins related to oxidative stress, all of which point to host-algal imbalance. This corroborates earlier metagenomic analysis of these samples, which found that infected colonies harbor a unique community of algae dominated by Symbiodinium necroappetens, while healthy colonies are dominated by Durusdinium trenchii and Breviolum spp.

When compared to previous transcriptomic studies, both common and unique molecular reactions were observed, emphasizing the significance of combining multiple "omics" approaches to comprehend coral diseases. The results indicate that SCTLD in D. labyrinthiformis is linked to early immune suppression, coral-algal imbalance, oxidative stress, and subsequent healing responses.