Investigating the roles of transforming growth factor-beta in immune response of Orbicella faveolata, a scleractinian coral

Fuess, Lauren E.; Butler, Caleb C.; Brandt, Marilyn E.; Mydlarz, Laura D.

doi:10.1016/j.dci.2020.103639

Cited by 14 publications

(11 citation statements)

References 68 publications

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“…Previous studies have suggested that symbiont may exploit host pathways such as TGFβ (Detournay et al, 2012;Berthelier et al, 2017) and the sphingosine rheostat (Detournay and Weis, 2011) to elicit changes in host coral gene expression, particularly as it relates to immunity. Furthermore, new findings suggest that TGFβ is capable of modulating immune response in O. faveolata (Fuess et al, 2020). Specifically, both toll-like receptor signaling (Naiki et al, 2005;Lee et al, 2011) and inflammation (Letterio and Roberts, 1998;Huynh et al, 2002) are intimately controlled by TGFβ signaling, and our results document significant negative correlations between symbiont density and these pathways.…”

Section: Discussionsupporting

confidence: 59%

Increased Algal Symbiont Density Reduces Host Immunity in a Threatened Caribbean Coral Species, Orbicella faveolata

et al. 2020

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Scleractinian corals are the principal builders of coral reefs. These megadiverse ecosystems are declining due to coral mortality from a variety of stressors, including disease. Corals are dependent upon symbiotic dinoflagellates in the family Symbiodiniaceae for phototrophic contributions to their energy budgets. However, suppression of host immunity may be necessary to maintain these intracellular symbioses. To explore the consequences of symbiosis on host immunity, we manipulated symbiont density by increasing nitrogen availability. Replicate cores from four colonies of the Caribbean coral, Orbicella faveolata, were reared in seawater treated with ammonium for 1 month to increase symbiont density. Corals were then immunestimulated using lipopolysaccharide and poly I:C. Gene expression was analyzed using RNAseq and symbiont density was quantified (as symbiont:host cell ratio) using quantitative PCR (qPCR). Ammonium treatment had limited positive effects on host immunity. In contrast, increases in symbiont density had large negative effects on host expression of immune-related transcripts. These results suggest links between nutrient enrichment and coral disease may be the result of the effect of increased symbiont density on host immunity, rather than the direct effect of the nutrients. Further study of the trade-offs between symbiont density and immunity may help understand how decreasing water quality and increasing disease will shape future reef communities.

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Section: Discussionsupporting

confidence: 59%

Increased Algal Symbiont Density Reduces Host Immunity in a Threatened Caribbean Coral Species, Orbicella faveolata

et al. 2020

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“…In both species the TGF-beta family genes associated with this orthogroup were downregulated (Supplementary Table 5). Previously, a study in O. faveolata found that exposure to exogenous TGF-beta had an immune suppressive effect, while inhibiting TGF-beta maintained the baseline immune response (Fuess et al, 2020). The downregulation of TGF-beta in both corals we hypothesize indicates that an immune response to SCTLD transmission is occurring.…”

Section: Shared Immune Activity In Both O Faveolata and M Cavernosamentioning

confidence: 50%

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

et al. 2021

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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.

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“…In fact, most transcriptomic studies of corals see changes in GO terms associated with immunity that may allow for more direct comparisons between different coral species and diseases. In several transcriptomic studies the GO terms for Immune Response Regulation and Innate Immunity (and variations within those) are typically enriched (Fuess et al, 2018(Fuess et al, , 2020Zhou et al, 2019;Takagi et al, 2020).…”

Section: Coral Immune Responses and Their Influences On Diseasementioning

confidence: 99%

Deciphering Coral Disease Dynamics: Integrating Host, Microbiome, and the Changing Environment

et al. 2020

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Diseases of tropical reef organisms is an intensive area of study, but despite significant advances in methodology and the global knowledge base, identifying the proximate causes of disease outbreaks remains difficult. The dynamics of infectious wildlife diseases are known to be influenced by shifting interactions among the host, pathogen, and other members of the microbiome, and a collective body of work clearly demonstrates that this is also the case for the main foundation species on reefs, corals. Yet, among wildlife, outbreaks of coral diseases stand out as being driven largely by a changing environment. These outbreaks contributed not only to significant losses of coral species but also to whole ecosystem regime shifts. Here we suggest that to better decipher the disease dynamics of corals, we must integrate more holistic and modern paradigms that consider multiple and variable interactions among the three major players in epizootics: the host, its associated microbiome, and the environment. In this perspective, we discuss how expanding the pathogen component of the classic host-pathogen-environment disease triad to incorporate shifts in the microbiome leading to dysbiosis provides a better model for understanding coral disease dynamics. We outline and discuss issues arising when evaluating each component of this trio and make suggestions for bridging gaps between them. We further suggest that to best tackle these challenges, researchers must adjust standard paradigms, like the classic one pathogen-one disease model, that, to date, have been ineffectual at uncovering many of the emergent properties of coral reef disease dynamics. Lastly, we make recommendations for ways forward in the fields of marine disease ecology and the future of coral reef conservation and restoration given these observations.

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Investigating the roles of transforming growth factor-beta in immune response of Orbicella faveolata, a scleractinian coral

Cited by 14 publications

References 68 publications

Increased Algal Symbiont Density Reduces Host Immunity in a Threatened Caribbean Coral Species, Orbicella faveolata

Increased Algal Symbiont Density Reduces Host Immunity in a Threatened Caribbean Coral Species, Orbicella faveolata

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

Deciphering Coral Disease Dynamics: Integrating Host, Microbiome, and the Changing Environment

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