Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25906400_1.fastq.gz | Fastqsanger.gz | |||
| SRR25906400_2.fastq.gz | Fastqsanger.gz | |||
| SRR25906401_1.fastq.gz | Fastqsanger.gz | |||
| SRR25906401_2.fastq.gz | Fastqsanger.gz | |||
| SRR25906402_1.fastq.gz | Fastqsanger.gz |
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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.
2020-12-18 | GSE124256 | GEO
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: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.
2024-12-10 | GSE232809 | GEO
Project description:Emergence of the symbiotic lifestyle fostered the immense diversity of all ecosystems on Earth, but symbiosis plays a particularly remarkable role in marine ecosystems. Photosynthetic dinoflagellate endosymbionts power reef ecosystems by transferring vital nutrients to their coral hosts. The mechanisms driving this symbiosis, specifically those which allow hosts to discriminate between beneficial symbionts and pathogens, are not well understood. Here, we uncover that host immune suppression is key for dinoflagellate endosymbionts to avoid elimination by the host using a comparative, model systems approach. Unexpectedly, we find that the clearance of non-symbiotic microalgae occurs by non-lytic expulsion (vomocytosis) and not intracellular digestion, the canonical mechanism used by professional immune cells to destroy foreign invaders. We provide evidence that suppression of TLR signalling by targeting the conserved MyD88 adapter protein has been co-opted for this endosymbiotic lifestyle, suggesting that this is an evolutionarily ancient mechanism exploited to facilitate symbiotic associations ranging from coral endosymbiosis to the microbiome of vertebrate guts.
2021-04-14 | GSE141133 | GEO
Project description:Emergence of the symbiotic lifestyle fostered the immense diversity of all ecosystems on Earth, but symbiosis plays a particularly remarkable role in marine ecosystems. Photosynthetic dinoflagellate endosymbionts power reef ecosystems by transferring vital nutrients to their coral hosts. The mechanisms driving this symbiosis, specifically those which allow hosts to discriminate between beneficial symbionts and pathogens, are not well understood. Here, we uncover that host immune suppression is key for dinoflagellate endosymbionts to avoid elimination by the host using a comparative, model systems approach. Unexpectedly, we find that the clearance of non-symbiotic microalgae occurs by non-lytic expulsion (vomocytosis) and not intracellular digestion, the canonical mechanism used by professional immune cells to destroy foreign invaders. We provide evidence that suppression of TLR signalling by targeting the conserved MyD88 adapter protein has been co-opted for this endosymbiotic lifestyle, suggesting that this is an evolutionarily ancient mechanism exploited to facilitate symbiotic associations ranging from coral endosymbiosis to the microbiome of vertebrate guts.
2021-04-14 | GSE140173 | GEO
Project description:The surprising observation that virtually the entire human genome is transcribed means we know very little about the function of many emerging classes of RNAs, except their astounding diversity. Traditional RNA function prediction methods rely on sequence or alignment information, which are limited in their ability to classify classes of non-coding RNAs (ncRNAs). To address this, we developed CoRAL, a machine learning-based approach for classification of RNA molecules. CoRAL uses biologically interpretable features including fragment length, cleavage specificity, and antisense transcription to distinguish between different ncRNA classes. We evaluated CoRAL using genome-wide small RNA sequencing (smRNA-seq) datasets from two human tissue types (brain and skin [GSE31037]), and were able to classify six different types of RNA transcripts with 79~80% accuracy in cross-validation experiments, and with 71~73% accuracy when CoRAL uses one tissue type for training and the other as validation. Analysis by CoRAL revealed that long intergenic ncRNAs, small cytoplasmic RNAs, and small nuclear RNAs show more tissue specificity, while microRNAs, small nucleolar, and transposon-derived RNAs are highly discernible and consistent across the two tissue types. The ability to consistently annotate loci across tissue types demonstrates the potential of CoRAL to characterize ncRNAs using smRNA-seq data in less characterized organisms.
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