Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1074944 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:Peritoneal carcinomatosis is a frequent finding in patients with primary gastric cancer, and it is associated with a poor prognosis. A major mechanism in peritoneal carcinomatosis is the dissemination of cancer cells into the abdominal cavity, mainly in diffuse gastric adenocarcinoma. The features that enable diffuse primary gastric tumours to develop peritoneal dissemination have been little investigated and are only incompletely understood. We therefore compared the gene expression profile in patients with diffuse primary gastric cancer with and without peritoneal carcinomatosis. Specimens from consecutive gastric cancer patients with and without peritoneal carcinomatosis were investigated using oligonucleotide microarrays. Keywords: Disease state analysis
2008-01-31 | GSE8657 | GEO
Project description:Microbiome dysregulation affects the estrogen metabolism (estrobolome) profile which in turns affects the immunological response. Estrogen hormone is an essential hormone that regulates the sexual activity in females as well as immune response in both sexes. Endometriosis is one of complicated disorder influnce the fertility of females due to escape of endometrial tissue into peritoneal cavity where the immunotoxicity will be undertaken. This study designed to investigate if there is any correlation between the microbiome dyregulation with the severity of endometriosis outcomes.
2023-12-08 | GSE248213 | GEO
Project description:Background Alterations of the gut microbiome have been linked to multiple chronic diseases. However, the drivers of such changes remain largely unknown. The oral cavity acts as a major route of exposure to exogenous factors including pathogens, and processes therein may affect the communities in the subsequent compartments of the gastrointestinal tract. Here, we perform strain-resolved, integrated multi-omic analyses of saliva and stool samples collected from eight families with multiple cases of type 1 diabetes mellitus (T1DM). Results We identified distinct oral microbiota mostly reflecting competition between streptococcal species. More specifically, we found a decreased abundance of the commensal Streptococcus salivarius in the oral cavity of T1DM individuals, which is linked to its apparent competition with the pathobiont Streptococcus mutans. The decrease in S. salivarius in the oral cavity was also associated with its decrease in the gut as well as higher abundances in facultative anaerobes including Enterobacteria. In addition, we found evidence of gut inflammation in T1DM as reflected in the expression profiles of the Enterobacteria as well as in the human gut proteome. Finally, we were able to follow transmitted strain-variants from the oral cavity to the gut at the metagenomic, metatranscriptomic and metaproteomic levels, highlighting not only the transfer, but also the activity of the transmitted taxa along the gastrointestinal tract. Conclusions Alterations of the oral microbiome in the context of T1DM impact the microbial communities in the lower gut, in particular through the reduction of “oral-to-gut” transfer of Streptococcus salivarius. Our results indicate that the observed oral-cavity-driven gut microbiome changes may contribute towards the inflammatory processes involved in T1DM. Through the integration of multi-omic analyses, we resolve strain-variant “mouth-to-gut” transfer in a disease context.
2022-10-05 | PXD031579 | Pride
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