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Brandt, M. E.

Publications and source records attributed to Brandt, M. E..

2 recordsLinked to original sources

Characterizing gene expression profiles of various tissue states in stony coral tissue loss disease using a feature selection algorithm

Stony coral tissue loss disease (SCTLD) remains a substantial threat to coral reef diversity already threatened by global climate change. Restoration efforts and effective treatment of SCTLD requires an in-depth understanding of its pathogenesis in the coral holobiont as well as mechanisms of disease resistance. Here, we present a supervised machine learning framework to describe SCTLD progression in a major reef-building coral, Montastraea cavernosa, and its dominant algal endosymbiont, Cladocopium goreaui. Utilizing support vector machine recursive feature elimination (SVM-RFE) in conjunction with differential expression analysis, we identify a subset of biologically relevant genes that exhibit the highest classification performance across three types of coral tissues collected from a natural reef environment: apparently healthy tissue on an apparently healthy colony, apparently healthy tissue on a SCTLD-affected colony, and lesion tissue on a SCTLD-affected colony. By analyzing gene expression signatures associated with these tissue health states in both the coral host and its algal endosymbiont (family Symbiodiniaceae), we describe key processes involved in SCTLD resistance and disease progression within the coral holobiont. Our findings further support evidence that SCTLD causes dysbiosis between the coral host and its Symbiodinaiceae and additionally describes the metabolic and immune shifts that occur as the holobiont transitions from a healthy to a diseased state. This supervised machine learning framework offers a novel approach to accurately assess the health states of endangered coral species and brings us closer to developing effective solutions for disease monitoring and intervention. AUTHOR SUMMARYCoral reefs are under increasing threat due to climate change, with rising ocean temperatures and disease outbreaks accelerating reef degradation. Stony coral tissue loss disease (SCTLD) has been particularly destructive, leading to widespread coral mortality across Floridas Coral Reef and the wider Caribbean since its emergence in 2014. While the cause of SCTLD remains unknown, the rapid decline in coral reef health highlights the urgent need for innovative approaches to understanding threats to coral health. In this study, we applied a supervised machine learning approach, previously used in cancer research, to identify key genes associated with SCTLD progression in the coral Montastraea cavernosa and its symbiotic algae, which the coral relies on to meet its nutritional requirements. By analyzing gene expression patterns across tissues representing different health states, we find that SCTLD affects the metabolic interactions between the coral and their symbionts and causes shifts in coral immune signaling pathways, even in tissue on a SCTLD-affected colony that appears to be healthy. This study presents a novel framework for applying supervised machine learning in coral gene expression research and could lead to new methods for monitoring coral health and combatting SCTLD.

genomics↗

A meta-analysis of the stony coral tissue loss disease microbiome finds key bacteria in lesions and unaffected tissue of diseased colonies

Stony coral tissue loss disease (SCTLD) has been causing significant whole colony mortality on reefs in Florida and the Caribbean. The cause of SCTLD remains unknown, with limited concurrence of SCTLD-associated bacteria among studies. We conducted a meta-analysis of SSU 16S ribosomal RNA gene datasets generated by 16 field and laboratory SCTLD studies to find consistent bacteria associated with SCTLD across disease zones (vulnerable, endemic, and epidemic), coral species, coral compartments (mucus, tissue, and skeleton), and disease states (apparently healthy colony tissue [AH], and unaffected [DU] and lesion [DL] tissue from diseased colonies). We also evaluated bacteria in seawater and sediment, which may be sources of SCTLD transmission. Although AH colonies in endemic and epidemic zones harbor bacteria associated with SCTLD lesions, and aquaria and field samples had distinct microbial compositions, there were still clear differences in the microbial composition among AH, DU, and DL in the combined dataset. Alpha diversity between AH and DL was not different; however, DU showed increased alpha diversity compared to AH, indicating that, prior to lesion formation, corals may undergo a disturbance to the microbiome. This disturbance may be driven by Flavobacteriales, which were especially enriched in DU. While Rhodobacterales and Peptostreptococcales-Tissierellales were prominent in structuring microbial interactions in DL. Peptostreptococcales-Tissierellales specifically may contribute to lesion progression through an alpha-toxin. We provide a consensus of SCTLD-associated bacteria both prior to and during lesion progression and identify how these taxa vary across studies, coral species, coral compartments, seawater, and sediment.

microbiology↗