Proteomic analysis of Stony Coral Tissue Loss Disease demonstrates coral-algal dysbiosis during disease progression
- 1Rutgers University
Abstract
Stony Coral Tissue Loss Disease (SCTLD) has devastated Caribbean reefs, yet the host molecular response to infection is poorly understood. Previous gene expression studies of diseased corals identified shifts in the immune response, apoptosis, and coral-algal dysbiosis. Here, we characterized the proteomic response of Diploria labyrinthiformis to SCTLD by comparing protein abundance in healthy tissue from uninfected colonies and apparently healthy and neighboring diseased tissue from infected colonies. These results were compared with existing metagenomic data from the same samples that previously demonstrated significant shifts in the coral microbiome due to SCTLD. We identified 480 differentially abundant proteins when comparing diseased lesion and healthy tissues, but only 12 between apparently healthy and healthy tissues. Pathway-level analysis provides evidence of immune suppression in apparently healthy tissue, suggesting that host molecular responses precede visible disease progression. Diseased lesion tissues showed wound-healing responses combined with a decreased abundance of proteins involved in symbiosome maintenance and increased oxidative stress responses, consistent with host-algal dysbiosis. This result correlates with the previous metagenomic analysis of these samples which found that infected colonies exhibit distinct algal symbiont communities dominated by Symbiodinium necroappetens, whereas healthy colonies are dominated by Durusdinium trenchii and Breviolum spp. Comparison with existing transcriptomic studies revealed both shared and distinct molecular responses, underscoring the importance of integrating multi-omics approaches to understand coral diseases. Our results suggest that SCTLD in D. labyrinthiformis is associated with early immune suppression, coral-algal dysbiosis, oxidative stress, and subsequent wound-healing responses.
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BibTeX
@misc{nandi2026proteomic,
title = {{Proteomic analysis of Stony Coral Tissue Loss Disease demonstrates coral-algal dysbiosis during disease progression}},
author = {S. Nandi and T. G. Stephens and K. H. Walsh and R. L. Garcia-Camps and M. F. Villalpando and R. I. Sellares and A. L. ZUBILLAGA and H. Zheng and A. Croquer and D. Bhattacharya},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.01.748617},
url = {https://www.biorxiv.org/content/10.64898/2026.09.01.748617v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Proteomic analysis of Stony Coral Tissue Loss Disease demonstrates coral-algal dysbiosis during disease progression
AU - S. Nandi
AU - T. G. Stephens
AU - K. H. Walsh
AU - R. L. Garcia-Camps
AU - M. F. Villalpando
AU - R. I. Sellares
AU - A. L. ZUBILLAGA
AU - H. Zheng
AU - A. Croquer
AU - D. Bhattacharya
PY - 2026
DA - 2026/09/01
PB - bioRxiv
DO - 10.64898/2026.09.01.748617
UR - https://www.biorxiv.org/content/10.64898/2026.09.01.748617v1
AB - Stony Coral Tissue Loss Disease (SCTLD) has devastated Caribbean reefs, yet the host molecular response to infection is poorly understood. Previous gene expression studies of diseased corals identified shifts in the immune response, apoptosis, and coral-algal dysbiosis. Here, we characterized the proteomic response of Diploria labyrinthiformis to SCTLD by comparing protein abundance in healthy tissue from uninfected colonies and apparently healthy and neighboring diseased tissue from infected colonies. These results were compared with existing metagenomic data from the same samples that previously demonstrated significant shifts in the coral microbiome due to SCTLD. We identified 480 differentially abundant proteins when comparing diseased lesion and healthy tissues, but only 12 between apparently healthy and healthy tissues. Pathway-level analysis provides evidence of immune suppression in apparently healthy tissue, suggesting that host molecular responses precede visible disease progression. Diseased lesion tissues showed wound-healing responses combined with a decreased abundance of proteins involved in symbiosome maintenance and increased oxidative stress responses, consistent with host-algal dysbiosis. This result correlates with the previous metagenomic analysis of these samples which found that infected colonies exhibit distinct algal symbiont communities dominated by Symbiodinium necroappetens, whereas healthy colonies are dominated by Durusdinium trenchii and Breviolum spp. Comparison with existing transcriptomic studies revealed both shared and distinct molecular responses, underscoring the importance of integrating multi-omics approaches to understand coral diseases. Our results suggest that SCTLD in D. labyrinthiformis is associated with early immune suppression, coral-algal dysbiosis, oxidative stress, and subsequent wound-healing responses.
ER -