4.5 Article

Identifying metabolic alterations associated with coral growth anomalies using 1H NMR metabolomics

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CORAL REEFS
卷 40, 期 4, 页码 1195-1209

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SPRINGER
DOI: 10.1007/s00338-021-02125-7

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Coral disease; Growth anomalies; Metabolomics; NMR spectroscopy; Porites compressa

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The study examined the metabolic impacts of Coral growth anomalies (GAs) through H-1 nuclear magnetic resonance (NMR) metabolomics, identifying 18 metabolites and indicating elevated metabolic activity in GA-impacted colonies. There was high variation in metabolomic profiles among coral samples, but features that differed between GA and unaffected samples were identified. Pathway analyses suggested decreased choline oxidation in GA samples, highlighting a pathway of interest for future targeted studies.
Coral growth anomalies (GAs) are tumor-like protrusions that are detrimental to coral health, affecting both the coral skeleton and soft tissues. These lesions are increasingly found throughout the tropics and are commonly associated with high human population density, yet little is known about the molecular pathology of the disease. Here, we investigate the metabolic impacts of GAs through H-1 nuclear magnetic resonance (NMR) metabolomics in Porites compressa tissues from a site of high disease prevalence (Coconut Island, Hawaii). We putatively identified 18 metabolites (8.1% of total annotated features) through complementary H-1 and H-1-C-13 heteronuclear single quantum correlation NMR data that increase confidence in pathway analyses and may bolster future coral metabolite annotation efforts. Extract yield was elevated in both GA and unaffected (normal tissue from a diseased colony) compared to reference (normal tissue from GA-free colony) samples, potentially indicating elevated metabolic activity in GA-impacted colonies. Relatively high variation in metabolomic profiles among coral samples of the same treatment (i.e., inter-colony variation) confounded data interpretation, however, analyses of paired GA and unaffected samples identified 73 features that differed between these respective metabolome types. These features were largely annotated as unknowns, but 1-methylnicotinamide and trigonelline were found to be elevated in GA samples, while betaine, glycine, and histamine were lower in GA samples. Pathway analyses indicate decreased choline oxidation in GA samples, making this a pathway of interest for future targeted studies. Collectively, our results provide unique insights into GA pathophysiology by showing these lesions alter both the absolute and relative metabolism of affected colonies and by identifying features (metabolites and unknowns) and metabolic pathways of interest in GA pathophysiology going forward.

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