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Tracey B. Schock

Publications and source records attributed to Tracey B. Schock.

2 recordsLinked to original sources

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

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 1 H 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 1 H and 1 H– 13 C 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.

Coral Reefs

Morphological, elemental, and boron isotopic insights into pathophysiology of diseased coral growth anomalies

Growth anomalies (GAs) impact both coral skeleton and soft tissues and are detrimental to reef health. This tumor-like disease is increasingly found throughout the tropics and is commonly associated with high human population density, yet little is known about the etiology, pathology, or calcification behavior of the disease. Here, we investigate potential mechanisms involved in the development of GAs through chemical and morphological characterization of GA skeletons in Porites compressa from a site of high disease prevalence (Coconut Island, Hawaii). A comprehensive suite of trace elements and boron isotopes (δ11B) were measured in skeletal GAs to assess calcification behavior and uptake of essential and toxic metals. Scanning electron microscopy of GA skeleton revealed it to be highly porous consisting of a matrix with a disorganized crystal structure, in contrast to the dense well-organized normal skeleton of P. compressa. Elemental analyses revealed decreased Mg/Ca and increased U/Ca in GA skeletons relative to paired unaffected samples, suggesting a decreased abundance of rapidly accreting microstructures “centers of calcification” in the GAs. Estimates of carbonate system parameters based on δ11B and B/Ca measurements indicate reduced pH (–0.05 units) and [CO32–] within the calcifying fluid of GAs, which may have implications for GA calcification. Higher levels of essential (V/Ca and Mo/Ca) elements in GAs potentially indicate increased abundance of holobiont-associated, nitrogen-fixing bacteria and higher Sb/Ca and Nd/Ca indicate alteration in the accumulation/depuration of these toxic metals. In aggregate, our findings show that dystrophic calcification processes could explain structural differences seen in GA vs unaffected skeletons and highlight the use of approaches herein to shed light on disease pathophysiology in corals.

Scientific Reports