Amphibian Metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA926636 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23242214_1.fastq.gz | Fastqsanger.gz | |||
| SRR23242214_2.fastq.gz | Fastqsanger.gz | |||
| SRR23242215_1.fastq.gz | Fastqsanger.gz | |||
| SRR23242215_2.fastq.gz | Fastqsanger.gz | |||
| SRR23242216_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 48 |
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Project description:Lead (Pb) is a widespread environmental toxicant that can elicit a wide variety of adverse effects in aquatic species. In fish, exposure to Pb can induce oxidative stress and reduce antioxidant capacity and there is evidence that Pb-induced developmental abnormalities are the result of dysregulated metabolism pathways but to date, no studies have characterised the molecular mechanisms of lead toxicity in amphibians. To investigate this, we coupled transcriptomic responses and early-life stage toxicity testing to identify specific molecular mechanisms that drive the adverse effects of lead, in Xenopus laevis. Embryos were exposed to one of the concentrations (0, 70, 210 and 630 ng/L) of lead (II) nitrate starting from 2 days post fertilization (dpf) until 6 dpf and 21 dpf to examine the transcriptomic and apical responses, respectively. We observed common dysregulated pathways and with similar magnitude at medium and high lead concentrations, but a phenotypic response only with the highest lead level. RNA Seq analysis showed about ~250 differentially expressed genes that could be further categorized into KEGG pathways based on their involvement in key biological processes. The most dysregulated pathways were Glutathione metabolism, Cytochrome P450 (drug/ xenobiotic metabolism) and Steroid hormone biosynthesis. Developmental studies showed that tadpoles exposed to the highest Pb concentration (630 ug/L) had significantly decreased total length and higher proportion of developmental abnormalities. Therefore, evaluating gene expression responses can provide early indication of toxicological mechanisms of lead effects in amphibians. As with fish, dysregulated metabolic pathways are most likely the molecular mechanisms underlying lead toxicity in ELS amphibians and contribute to the altered growth and developmental abnormalities observed in this study.
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Project description:<p>Diet is a major determinant of gut microbiome composition, and variation in diet-microbiome interactions may contribute to variation in their health consequences. Understanding individual differences requires mechanistic understanding of dietary xenobiotics-microbiome interactions. Here, we map interactions between ~150 small molecule dietary xenobiotics and the gut microbiome, including community composition, compound metabolism, growth inhibitory effects and interindividual variation in these traits. Integrating these measures highlights mechanisms for community remodelling. We identify dietary xenobiotics with growth inhibitory activity and demonstrate how these compounds alter community composition. Microbial metabolism both toxifies and detoxifies these compounds, producing emergent interactions. We identify the gene and enzyme responsible for detoxification of one such dietary xenobiotic, resveratrol, and demonstrate that this enzyme contributes to interindividual variation in community remodelling. Together, these results systematically map interactions between dietary xenobiotics and the gut microbiome and suggest how toxification and detoxification contributes to interpersonal differences in microbiome response to diet.</p>
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Project description:Tert-Butylhydroquinone (tBHQ), a preservative used to prevent oxidative deterioration of oil, fat, and meat products, has been linked to both chemoprotective and adverse effects. This study investigates the impact of chronic dietary tBHQ on survival, growth parameters, organ development, and gene expression in zebrafish (Danio rerio). As tBHQ activates the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2a), a zebrafish line with a mutation in the DNA-binding domain was used to identify Nrf2a-dependent vs. independent effects. Homozygous Nrf2a wildtype (wt) and mutant (m) larvae were fed a diet containing 5% tBHQ or a control diet. Survival and growth parameters were assessed at 15 days and at 5 months, and samples collected for RNA sequencing at 5 months. Chronic dietary exposure to tBHQ throughout the larval and juvenile periods negatively impacted growth and survival. RNA-seq analysis found differentially expressed genes related to growth and development and upregulation of several immune pathways. The findings herein demonstrate that chronic dietary tBHQ exposure may impair growth and survival in both Nrf2a dependent and independent manners.
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Project description:Reed2004 - Methionine Cycle
This model is described in the article:
A mathematical model of the
methionine cycle.
Reed MC, Nijhout HF, Sparks R,
Ulrich CM.
J. Theor. Biol. 2004 Jan; 226(1):
33-43
Abstract:
Building on the work of Martinov et al. (2000), a
mathematical model is developed for the methionine cycle. A
large amount of information is available about the enzymes that
catalyse individual reaction steps in the cycle, from
methionine to S-adenosylmethionine to S-adenosylhomocysteine to
homocysteine, and the removal of mass from the cycle by the
conversion of homocysteine to cystathionine. Nevertheless, the
behavior of the cycle is very complicated since many substrates
alter the activities of the enzymes in the reactions that
produce them, and some can also alter the activities of other
enzymes in the cycle. The model consists of four differential
equations, based on known reaction kinetics, that can be solved
to give the time course of the concentrations of the four main
substrates in the cycle under various circumstances. We show
that the behavior of the model in response to genetic
abnormalities and dietary deficiencies is similar to the
changes seen in a wide variety of experimental studies. We
conduct computational "experiments" that give understanding of
the regulatory behavior of the methionine cycle under normal
conditions and the behavior in the presence of genetic
variation and dietary deficiencies.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000698.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000698 | BioModels