Ontology highlight
ABSTRACT:
PROVIDER: PRJNA390196 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5677670.fastq.gz | Fastqsanger.gz | |||
| SRR5677680.fastq.gz | Fastqsanger.gz | |||
| SRR5677690.fastq.gz | Fastqsanger.gz | |||
| SRR5677700.fastq.gz | Fastqsanger.gz | |||
| SRR5677671.fastq.gz | Fastqsanger.gz |
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Project description:Florida’s coral reefs are currently experiencing a multi-year disease-related mortality event, that has resulted in massive die-offs in multiple coral species. Approximately 21 species of coral, including both Endangered Species Act-listed and the primary reef-building species, have displayed tissue loss lesions which often result in whole colony mortality [Stony Coral Tissue Loss Disease (SCTLD)]. Determining the causative agent(s) of coral disease relies on a multidisciplinary approach since the causation may be a combination of abiotic, microbial or viral agents. Metaproteomics was used to survey changes in the molecular landscape in the coral holobiont with the goal of providing useful information not only in diagnosis, but for prediction and prognosis. Specifically, in the case of SCTLD, defining molecular changes in the coral holobiont will help define disease progression and aid in identifying the causative agent by clearly defining traits of disease progression shared across affected species. Using samples from nine coral species (46 samples total; those appearing healthy, n = 23, and diseased, n = 23), analysis of the coral and its associated microbiome were performed using bottom-up proteomics. Ongoing analysis (including improving coral holobiont genome-based search space) will demonstrate the utility of this approach and help define improved future experiments.
2021-05-21 | PXD026192 | Pride
Project description:Branching coral species like the Caribbean Acroporids are long lived and reproduce asexually via breakage of branches. Fragmentation is the dominant mode of local population maintenance for these corals across much of their range. Thus, large genets with many member ramets (colonies) are common. Each of the ramets experiences different microenvironments, especially with respect to light and water flow. Here, we investigate whether colonies that are members of the same genet have different epigenomes because of differences in their microenvironments. The Florida Keys experienced a large- scale coral bleaching event in 2014-2015 caused by high water temperatures. During the event, ramets of the same coral genet bleached differently. Previous work had shown that this was unlikely to be due to their eukaryotic algal symbionts (Symbiodinium ‘fitti’) because each genet of this coral species typically harbors a single strain of S. ‘fitti’. Characterization of the microbiome via 16S tag sequencing did not provide evidence for a central role of microbiome variation in determining bleaching response. Instead, epigenetic changes were significantly correlated with the host’s genetic background, the position of the sampled polyps within the colonies (e.g. tip versus base of colony), and differences in the colonies’ condition during the bleaching event. We conclude that microenvironmental differences in growing conditions led to long-term changes in the way the ramets methylated their genomes and thus to a differential bleaching response.
2019-12-05 | GSE124246 | GEO
Project description:Branching coral species like the Caribbean Acroporids are long lived and reproduce asexually via breakage of branches. Fragmentation is the dominant mode of local population maintenance for these corals across much of their range. Thus, large genets with many member ramets (colonies) are common. Each of the ramets experiences different microenvironments, especially with respect to light and water flow. Here, we investigate whether colonies that are members of the same genet have different epigenomes because of differences in their microenvironments. The Florida Keys experienced a large- scale coral bleaching event in 2014-2015 caused by high water temperatures. During the event, ramets of the same coral genet bleached differently. Previous work had shown that this was unlikely to be due to their eukaryotic algal symbionts (Symbiodinium ‘fitti’) because each genet of this coral species typically harbors a single strain of S. ‘fitti’. Characterization of the microbiome via 16S tag sequencing did not provide evidence for a central role of microbiome variation in determining bleaching response. Instead, epigenetic changes were significantly correlated with the host’s genetic background, the position of the sampled polyps within the colonies (e.g. tip versus base of colony), and differences in the colonies’ condition during the bleaching event. We conclude that microenvironmental differences in growing conditions led to long-term changes in the way the ramets methylated their genomes and thus to a differential bleaching response.
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Project description:Corals rely on a symbiosis with dinoflagellate algae (Symbiodinium spp.) to thrive in nutrient poor tropical oceans. However, the coral-algal symbiosis can break down during bleaching events, potentially leading to coral death. While genome-wide expression studies have shown the genes associated with the breakdown of this partnership, the full conglomerate of genes responsible for the establishment and maintenance of a healthy symbiosis remains unknown. Results from previous studies suggested little transcriptomic change associated with the establishment of symbiosis. In order to elucidate the transcriptomic response of the coral host in the presence of its associated symbiont, we utilized a comparative framework. Post-metamorphic aposymbiotic coral polyps of Orbicella faveolata were compared to symbiotic coral polyps 9 days after metamorphosis and the subsequent differential gene expression between control and treatment was quantified using cDNA microarray technology. Coral polyps exhibited differential expression of genes associated with nutrient metabolism and development, providing insight into pathways turned as a result of symbiosis driving early polyp growth. Furthermore, genes associated with lysosomal fusion were also upregulated, suggesting host regulation of symbiont densities soon after infection.
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Project description:The bacterial pathogen Vibrio coralliilyticus infects a variety of marine organisms globally and causes early onset of disease in multiple coral species. The etiology of coral disease and relative pathogenicity of V. coralliilyticus strains is well-documented, but the mechanisms of V. coralliilyticus coral colonization, virulence factor production, and interactions with coral microbiome are understudied. Many virulence factors responsible for pathogenic behaviors are controlled through a density-dependent, bacterial communication system called quorum sensing (QS). In other Vibrio species, behaviors like bioluminescence, biofilm formation, toxin secretion, and protease production are controlled via the master quorum sensing transcriptional regulator called LuxR/HapR. Comparative genomics indicated that V. coralliilyticus genomes share high sequence identity for most of the QS signaling and regulatory components identified in other Vibrio species. Here, we characterize active components of the V. coralliilyticus QS system and identify the VcpR (LuxR/HapR homolog) regulons in two strains with distinct infection etiologies. We show that VcpR transcription is dependent on signaling by autoinducer AI-2, whereas we were unable to detect production of acyl-homoserine lactone autoinducers. The VcpR regulator controls expression of >200 genes in both the type strain BAA-450 and isolate OCN008, including two genes encoding proteases (VcpA and VcpB) known to impact coral infection. In both isolates, VcpR activates the expression of Type VI Secretion System genes from both systems 1 and 2, which results in interbacterial competition and killing of prey bacteria. We conclude that the QS system in V. coralliilyticus is active and controls expression of genes involved in relevant bacterial behaviors that may influence coral infection.
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Project description:We explore whether a low-energy diet intervention for Metabolic dysfunction-associated steatohepatitis (MASH) improves liver disease by means of modulating the gut microbiome. 16 individuals were given a low-energy diet (880 kcal, consisting of bars, soups, and shakes) for 12 weeks, followed by a stepped re-introduction to whole for an additional 12 weeks. Stool samples were obtained at 0, 12, and 24 weeks for microbiome analysis. Fecal microbiome were measured using 16S rRNA gene sequencing. Positive control (Zymo DNA standard D6305) and negative control (PBS extraction) were included in the sequencing. We found that low-energy diet improved MASH disease without lasting alterations to the gut microbiome.
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