Gene Expression Response to Stony Coral Tissue Loss Disease Transmission in M. cavernosa and O. faveolata From Florida

Abstract

Since 2014, corals within Florida’s Coral Reef have been dying at an unprecedented rate due to stony coral tissue loss disease (SCTLD). Here we describe the transcriptomic outcomes of three different SCTLD transmission experiments performed at the Smithsonian Marine Station and Mote Marine Laboratory between 2019 and 2020 on the corals Orbicella faveolata and Montastraea cavernosa. Overall, diseased O. faveolata had 2194 differentially expressed genes (DEGs) compared with healthy colonies, whereas diseased M. cavernosa had 582 DEGs compared with healthy colonies. Many significant DEGs were implicated in immunity, extracellular matrix rearrangement, and apoptosis. These included, but not limited to, peroxidases, collagens, Bax-like, fibrinogen-like, protein tyrosine kinase, and transforming growth factor beta. A gene module was identified that was significantly correlated to disease transmission. This module possessed many apoptosis and immune genes with high module membership indicating that a complex apoptosis and immune response is occurring in corals during SCTLD transmission. Overall, we found that O. faveolata and M. cavernosa exhibit an immune, apoptosis, and tissue rearrangement response to SCTLD. We propose that future studies should focus on examining early time points of infection, before the presence of lesions, to understand the activating mechanisms involved in SCTLD.

Disease resistance in coral is mediated by distinct adaptive and plastic gene expression profiles

“…Previous studies on coral disease and immunity have successfully identified genes induced by disease that contribute to biological processes such as apoptosis, autophagy, extracellular matrix maintenance, lipid metabolism, and protein trafficking (18)(19)(20)(21)(22). However, comparing immune responses between coral species that differ in disease resistance or susceptibility, linking specific disease phenotypes to gene expression, and determining adaptive or plastic disease resistance-associated expression patterns are understudied.…”

Divergent transcriptional response to thermal stress among life stages could constrain coral adaptation to climate change

“…Although functional genomic evidence for pleiotropy is currently lacking for corals, bleaching resistance in adults can come at the cost of other fitness-related traits (Cornwell et al, 2021; Shore-Maggio et al, 2018), suggesting pleiotropy can constrain thermal adaptation within life stages. Putatively pleiotropic genes identified in the present study include tumor necrosis factor receptor superfamily 19 and a peroxidasin homolog, which have been previously implicated as key players in both the immune (Traylor-Knowles et al, 2021) and environmental stress response (Barshis et al, 2013b; Louis et al, 2017) in coral, yet their role in developmental modulation is unknown. The present study provides the first evidence for developmental pleiotropy in corals at a molecular level and emphasizes the need for functional and quantitative genetics to be conducted across multiple life stages to determine the costs and limits of thermal adaptation.…”

Evolutionary responses of a reef-building coral to climate change at the end of the last glacial maximum

“…Peroxinectins are best characterised in arthropods where they mediate the immune response via cell adhesion (Johansson et al 1995) and prostaglandin synthesis (Park et al 2014). Heat stress experiments in molluscs (Lang et al 2009), and corals (Voolstra et al 2009; Shinzato et al 2021; Traylor-Knowles et al 2021) consistently identify peroxinectin-like proteins as differentially expressed, and there is evidence that they have undergone recent expansion in some heat-tolerant coral lineages (Shinzato et al 2021). Unfortunately the role of peroxinectins in corals has been obscured because many peroxinectin-like proteins are annotated as peroxidasin homologues in the NCBI nr database.…”