Starfish metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA432509 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6662010_1.fastq.gz | Fastqsanger.gz | |||
| SRR6662010_2.fastq.gz | Fastqsanger.gz | |||
| SRR6662020_1.fastq.gz | Fastqsanger.gz | |||
| SRR6662020_2.fastq.gz | Fastqsanger.gz | |||
| SRR6662030_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 180 |
Similar Datasets
Project description:Marine organisms represent a rich source for discovering natural products and materials that could inspire the development of novel molecules or materials for a high variety of industrial applications. Among them are sea stars, emblematic animals of the seashore. These organisms rely on epidermal secretions to cope with their benthic life. Their integument produces a mucus, which represents the first barrier against invaders; and their tube feet produce adhesive secretions to pry open mussels and attach strongly but temporarily to rocks. In this study, we investigate for the first time the protein content of mucous and adhesive secretions from the sea star Asterias rubens. These secretomes were analysed using tandem mass spectrometry and resulting MS/MS data were searched against in silico translated tube foot transcriptome. Tube foot transcripts coding for proteins identified in the two secretions were then functionally annotated by similarity searches against NCBI nr database.
2015-07-20 | PXD001607 | Pride
Project description:An Initial Comparative Genomic Autopsy of Wasting Disease in Sea Stars
| PRJNA603587 | ENA
Project description:Beginning in 2013, sea stars throughout the Eastern North Pacific were decimated by wasting disease, also known as ‘asteroid idiopathic wasting syndrome’ (AIWS) due to its elusive etiology. The geographic extent and taxonomic scale of AIWS meant events leading up to the outbreak were heterogeneous, multifaceted, and oftentimes unobserved; progression from morbidity to death was rapid, leaving few tell-tale symptoms. Here we take a forensic genomic approach to discover candidate genes that may help explain sea star wasting syndrome. We report the first genome and annotation for P. ochraceus, along with differential gene expression (DGE) analyses in four size classes, three tissue types, and in symptomatic and asymptomatic individuals. We integrate nucleotide polymorphisms associated with survivors of the wasting disease outbreak, DGE associated with temperature treatments in P. ochraceus, and DGE associated with wasting in another asteroid Pycnopodia helianthoides. In P. ochraceus, we find DGE across all tissues, among size classes, and between asymptomatic and symptomatic individuals; the strongest wasting-associated DGE signal is in pyloric caecum. We also find previously identified outlier loci co-occur with differentially expressed genes. In cross-species comparisons of symptomatic and asymptomatic individuals, consistent responses distinguish genes associated with invertebrate innate immunity and chemical defense, consistent with context-dependent stress responses, defensive apoptosis, and tissue degradation. Our analyses thus highlight genomic constituents that may link suspected environmental drivers (elevated temperature) with intrinsic differences among individuals (age/size, alleles associated with susceptibility) that elicit organismal responses (e.g. coelomocyte proliferation) and manifest as sea star wasting mass mortality.
2020-02-19 | GSE144422 | GEO
Project description:Sea stars and sea urchins are model systems for interrogating the types of deep evolutionary changes that have restructured developmental gene regulatory networks (GRNs). While cis regulatory DNA evolution is likely the predominant mechanism of change, it was recently shown that Tbrain, a Tbox transcription factor protein, has evolved a changed preference for a low affinity, secondary binding motif, although the primary, high affinity motif is conserved. To date, however, no genome-wide comparisons have been performed in order to provide an unbiased assessment of the evolution of GRNs between these taxa; and no study has attempted to determine the interplay between transcription factor binding motif evolution and GRN topology. The study here measures genome-wide binding of Tbrain orthologs using ChIP-seq, and associates these with putative target genes to assess global function. Targets of both factors are enriched for other regulatory genes, although non-overlapping sets of functional enrichments in the two datasets suggest a much diverged function. The number of low affinity binding motifs are significantly depressed in sea urchins compared to sea star, but both motifs types are associated with genes from a range of functional categories. Only a small fraction (~10%) of genes are predicted to be orthologous targets. Collectively these data indicate that Tbr has evolved significantly different developmental roles in these echinoderms, and that the maintained and unique targets, and their associated binding motifs are dispersed throughout the hierarchy of the GRN, rather than being biased towards terminal process or discrete functional blocks suggesting extensive evolutionary tinkering.
2016-12-01 | GSE89862 | GEO
Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.
2020-11-30 | E-MTAB-8739 | biostudies-arrayexpress
Project description:Protein profiling offers an effective approach to characterizing the departure from normal of epidermis in disease states. The present investigation tested the hypothesis that the differentiation of epidermal corneocytes is perturbed in the forehead of subjects exhibiting frontal fibrosing alopecia. To this end, samples were collected by tape stripping from subjects diagnosed with this condition and compared to those from asymptomatic control subjects and from those exhibiting androgenetic alopecia. Unlike the latter, which exhibited only 3 proteins significantly different from controls, forehead samples from frontal fibrosing alopecia subjects displayed 72 proteins significantly different from controls, nearly two-thirds having lower expression. Comparison to corresponding profiles in scalp samples from frontal fibrosing alopecia and androgenetic alopecia suggested the perturbation of epidermal differentiation in the former was even greater in the scalp.
2022-08-16 | MSV000090141 | MassIVE
Project description:Background: Atopic dermatitis (AD) is a common inflammatory skin disease exhibiting a predominantly Th2/"T22" immune activation and a defective epidermal barrier. Narrow-band UVB (NB-UVB) is considered an efficient treatment for moderate to severe AD. In psoriasis, NB-UVB has been found to suppress the Th1/Th17 immune polarization with subsequent reversal of epidermal hyperplasia. The immunomodulatory effects of this treatment are largely unknown in AD. Our study evaluates the effects of NB-UVB on immune and barrier abnormalities in AD, aiming to establish reversibility of disease and biomarkers of therapeutic response. Methods: 12 moderate-to-severe chronic AD patients received NB-UVB phototherapy 3 times weekly for up to 12 weeks. Lesional and non-lesional skin biopsies were obtained before and after treatment and evaluated by gene-expression and immunohistochemistry studies. Results: All patients had at least a 50% reduction in SCORing of AD (SCORAD) index with NB-UVB phototherapy. The Th2, T22, and Th1 immune pathways were suppressed and measures of epidermal hyperplasia and differentiation also normalized after phototherapy. The reversal of disease activity was associated with elimination of inflammatory leukocytes, Th2/"T22"-associated cytokines and chemokines, and normalized expression of barrier proteins. Conclusions: Our study shows reversal of both the epidermal defects and underlying immune activation in AD. By determining the correlation of variables with therapeutic response, we have defined a set of biomarkers of disease response that associate resolved Th2 and T22 inflammation with reversal of barrier pathology. This data supports the "inside-out" hypothesis of AD, suggesting that it is a disease primarily driven by an immune stimulus. genomic profiling of treatment effect of NB-UVB in AD in both lesional and non-lesional AD skin from 10 patients. Treatment effect, disease state analysis
2011-07-01 | E-GEOD-27887 | biostudies-arrayexpress