Ontology highlight
ABSTRACT:
PROVIDER: PRJNA542491 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9045600.fastq.gz | Fastqsanger.gz | |||
| SRR9045610.fastq.gz | Fastqsanger.gz | |||
| SRR9045601.fastq.gz | Fastqsanger.gz | |||
| SRR9045602.fastq.gz | Fastqsanger.gz | |||
| SRR9045603.fastq.gz | Fastqsanger.gz |
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Project description:To investigate mechanisms of metal tolerance in the gill, gut, kidney and liver of brown trout inhabiting the river Hayle (highly metal contaminated) compared with a control population from the river Teign. mRNA samples were sequenced (Illumina GAII) from a pooled embryonic sample and 12 multiplexed samples of different tissues from the the Hayle and Teign populations (pooled from 5 and 10 individuals respectively) and used to generate a transcriptome assembly. Expression profiling was then conducted for the gill, gut, kidney and liver samples. Expression profiling results are presented in this Series.
2014-06-01 | E-GEOD-45637 | biostudies-arrayexpress
Project description:The proliferative darkening syndrome (PDS) is an annually recurring disease that causes species-specific die-off of brown trout (Salmo trutta fario) in PDS-impacted pre-alpine rivers of central Europe. The mortality rate for PDS is near 100% and consequently the survival of brown trout populations in the impacted regions is threatened. The progression of PDS occurs in two stages, a subclinical stage and a symptomatic stage, over a time period of more than 3 months starting in spring and culminating with the die-off of brown trout in late summer. Based on experimental evidence it is hypothesized that PDS is caused by an infectious agent. To substantiate this working hypothesis as well as to discern the type of pathogen likely to be responsible for PDS, microarray analysis were conducted using a salmonid-specific cDNA microarray to assess the hepatic immune response of brown trout during the progression of PDS in 7-day intervals over a time period of 98 days.The microarray analysis revealed that brown trout suffering from PDS exhibit increased hepatic expression of important anti-viral genes both during the subclinical stage of PDS, namely the Barrier-to-autointegration factor, and during the symptomatic stage of PDS, namely the interferon regulatory factor 1 as well as the Guanylate-binding protein 1. Additionally, during the symptomatic stage of PDS there is strong hepatic up-regulation of the chemokine CCL19, complement components C1QC and C6, Proteasome activator complex subunits 1 and 2 as well as a variety of both MHC class I and MHC class II transcripts. In conclusion, the increased expression of hepatic immune response genes involved in a variety of immune system processes that mediate defense against infection identified by the microarray analysis during the progression of PDS support the working hypothesis that PDS is caused by an infectious agent. Furthermore, the up-regulation of antiviral immune response genes during both the subclinical stage and the symptomatic stage of PDS suggests that this disease is caused by a pathogenic virus. On May 29, 2008, brown trout (Salmo trutta fario) of the same age class (1+) with an individual weight ranging between 25-85 grams were obtained from a single hatchery (Schwäbischer Fischereihof Salgen, Fachberatung für Fischerei Schwaben, Germany) and randomly allocated to one of two different experimental stations that are both located along the Iller river, named here simply the control station (location by Oberstdorf, Germany) and the treatment station (location by Kempten, Germany). At both experimental stations brown trout were held in tanks (n=750 at the treatment station and n=70 at the control station) that were supplied with water from the Iller river in a flow-through system. Sampling at both experimental stations started on May 29, 2008, which was also the day on which the fish were first transferred to their exposure tanks (referred to as 0 day post exposure; d.p.e), and ended on the 5th of September 2008. At the treatment station 3 fish were sampled each day (always at 2pm), whereas at the control station 3 fish were sampled in 7-day intervals (always at 12 noon). Fish were anaesthetized by a blow to the head and organ tissue of interest (liver, kidney, spleen, gill, muscle, stomach and foregut tissue) were immediately harvested from sacrificed fish, snap-frozen in liquid nitrogen and subsequently stored at -80°C. Livers from the three brown trout (n=3) that were sampled concurrently from both treatment and control group (n=2) in 7-day intervals starting 7 d.p.e (7, 14, 21, 28, 35, 42, 49, 56, 63, 70, 77, 84, 91 and 98 d.p.e; n=14) were recruited for the use in the microarray analysis. Microarray analyses were performed using a direct comparison two-channel design in which equimolar amounts of liver sample of one brown trout from both treatment and control group were co-hybridized on the same microarray. For each time point (n=14) microarray co-hybridizations were repeated in triplicate (n=3) and included one dye-swap in order to reduce dye-bias. Thus a total of 42 microarray slides were used in this study (3 biological replicate microarrays x 14 time points = 42 microarrays).
2015-06-26 | E-GEOD-70257 | biostudies-arrayexpress
Project description:To investigate mechanisms of metal tolerance in the gill, gut, kidney and liver of brown trout inhabiting the river Hayle (highly metal contaminated) compared with a control population from the river Teign.
2014-06-01 | GSE45637 | GEO
Project description:The myxozoan Tetracapsuloides bryosalmonae is the causative agent of proliferative kidney disease (PKD) – a disease of salmonid fishes, notably of the commercially farmed rainbow trout Oncorhynchus mykiss. Both wild and farmed salmonids are threatened by this virulent/deadly disease, which is often expressed by swollen kidneys. In order to understand the causes and consequences of the disease, we studied the immune response towards the parasite. To profile the influence of the disease on these cells, we produced a transcriptome of teleost RBCs in health and disease. Compared to erythrocytes originating from healthy fish, PKD fundamentally altered RBCs in their metabolism, adhesion, and response to inflammation.
2022-08-31 | GSE198859 | GEO
Project description:These studies aimed to investigate the hepatic transcriptional response of brown trout to the natural estrogen, E2, and the herbicide linuron. We exposed mature male brown trout to three concentrations of each chemical for 4 days and sequenced the hepatic transcriptome of 3 individuals per treatment group in order to determine the global mechanisms of toxicity of these environmental contaminants. We assembled the brown trout transcriptome using a de novo approach. Subsequent differential expression analysis identified a total of 2113 differentially-regulated transcripts in the group exposed to the highest E2 treatment concentration, and 822 differentially-regulated transcripts across all linuron treatments. For E2, differentially-expressed transcripts included those encoding known oestrogen-responsive genes, while regulated processes included those associated with vitellogenesis including lipid metabolism, cellular proliferation and ribosome biogenesis. For linuron, there was a striking down-regulation of transcripts encoding the majority of the enzymes involved in the cholesterol biosynthesis pathway, and also a considerable induction of transcripts involved in cellular stress response including Cyp1a. Fish were exposed to 3 concentrations of E2 (measured concentrations were 1.9, 18.1 and 34.4 ng/L), 3 concentrations of linuron (measured concentrations were 1.7, 15.3 and 225.9 µg/L) and water controls for 4 days. Liver mRNA from 3 replicate individuals per treatment was sequenced in an Illumina HiSeq 2500 platform. Two control groups (n=6 fish in total) were included. Using a de novo approach, we assembled the hepatic transcriptome for brown trout. Sequence reads were re-mapped to the assembled transcriptome using Bowtie2 and transcript expression profiling was conducted using EdgeR. ERCC spike controls were added to all individual samples, allowing for the assessment of the reproducibility and dynamic range for transcript expression quantification in our experiments.
2015-05-08 | E-GEOD-57490 | biostudies-arrayexpress
Project description:These studies aimed to investigate the hepatic transcriptional response of brown trout to the natural estrogen, E2, and the herbicide linuron. We exposed mature male brown trout to three concentrations of each chemical for 4 days and sequenced the hepatic transcriptome of 3 individuals per treatment group in order to determine the global mechanisms of toxicity of these environmental contaminants. We assembled the brown trout transcriptome using a de novo approach. Subsequent differential expression analysis identified a total of 2113 differentially-regulated transcripts in the group exposed to the highest E2 treatment concentration, and 822 differentially-regulated transcripts across all linuron treatments. For E2, differentially-expressed transcripts included those encoding known oestrogen-responsive genes, while regulated processes included those associated with vitellogenesis including lipid metabolism, cellular proliferation and ribosome biogenesis. For linuron, there was a striking down-regulation of transcripts encoding the majority of the enzymes involved in the cholesterol biosynthesis pathway, and also a considerable induction of transcripts involved in cellular stress response including Cyp1a.
2015-05-08 | GSE57490 | GEO
Project description:To date, little is known about the proteomic changes at the portals of entry in rainbow trout after infection with the myxozoans, Myxobolus cerebralis, and Tetracapsuloides bryosalmonae the causative agents of whirling disease and proliferative kidney disease, respectively. Therefore, the aim of this study was to provide the first proteomic profiles of the host in the search for evasion strategies against single and coinfection with M. cerebralis and T. bryosalmonae. One group of fish was initially infected with M. cerebralis and another group with T. bryosalmonae. After 30 days, half of the fish in each group were co-infected with the other parasite. Using a quantitative proteomic approach, we investigated proteomic changes in the caudal fins and gills of rainbow trout before and after co-infection. In the caudal fins, 16 proteins were differentially regulated post exposure to M. cerebralis, whereas 27 proteins were differentially modulated in the gills of the infected rainbow trout post exposure to T. bryosalmonae. After co-infection, 4 proteins involved in parasite recognition and the regulation of host immune responses were differentially modulated between the groups in the caudal fin. In the gills, 11 proteins involved in parasite recognition and host immunity, including 4 myxozoan proteins predicted to be virulence factors, were differentially modulated. The results of this study increase our knowledge on rainbow trout co-infections by myxozoan parasites and rainbow trout immune responses against myxozoa at the portals of entry, supporting a better understanding of these host-parasite interactions.
2024-05-06 | PXD050412 | Pride
Project description:The proliferative darkening syndrome (PDS) is an annually recurring disease that causes species-specific die-off of brown trout (Salmo trutta fario) with a mortality rate of near 100 % in pre-alpine rivers of central Europe. So far the etiology and causation of this disease is still unclear. The objective of this study was to identify the cause of PDS using a next-generation technology detection pipeline. Following the hypothesis that PDS is caused by an infectious agent, brown trout specimens were exposed to water from a heavily affected pre-alpine river with annual occurrence of the disease. Specimens were sampled over the entire time period from potential infection through death. Transcriptomic analysis (microarray) and RT-qPCR of brown trout liver tissue evidenced strong gene expression response of immune-associated genes. Messenger RNA of specimens with synchronous immune expression profiles were ultra-deep sequenced using next-generation sequencing technology (NGS). Bioinformatic processing of generated reads and gap-filling Sanger re-sequencing of the identified pathogen genome revealed strong evidence that a piscine-related reovirus is the causative organism of PDS. The identified pathogen is phylogenetically closely related to the family of piscine reoviruses (PRV) which are considered as the causation of different fish diseases in Atlantic and Pacific salmonid species such as Salmo salar and Onchorhynchus kisutch. This study also highlights that the approach of first screening immune responses along a timeline in order to identify synchronously affected stages in different specimens which subsequently were ultra-deep sequenced is an effective approach in pathogen detection. In particular, the identification of specimens with synchronous molecular immune response patterns combined with NGS sequencing and gap-filling re-sequencing resulted in the successful pathogen detection of PDS.
2015-06-26 | GSE70257 | GEO