Pastureland metagenomes from Argentina
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB22053 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2071890_1.fastq.gz | Fastqsanger.gz | |||
| ERR2071890_2.fastq.gz | Fastqsanger.gz | |||
| ERR2071900_1.fastq.gz | Fastqsanger.gz | |||
| ERR2071900_2.fastq.gz | Fastqsanger.gz | |||
| ERR2071891_1.fastq.gz | Fastqsanger.gz |
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Project description:Epidemiological evidence suggests that people chronically exposed to organophosphorus pesticides are at increased risk of neurodegenerative disease. Covalently linked amyloid beta dimers have been isolated from the brains of Alzheimer’s patients. The toxic forms of amyloid beta are amyloid dimers that spontaneously oligomerize. In the present report we treated recombinant and synthetic amyloid beta (1-42) with 1 mM chlorpyrifos oxon or 1 mM paraoxon. The trypsin-digested samples were analyzed by liquid chromatography tandem mass spectrometry on an Orbitrap Fusion Lumos mass spectrometer. Data were searched with Protein Prospector software. We found two new types of crosslinks in amyloid dimers. An isopeptide Asp-Asp link occurred between the N-terminal amine of Asp 1 in one peptide and the beta carboxyl group of Asp 1 in another peptide. An Asp-Arg link occurred between the guanidino group of Arg 5 in one peptide and the beta carboxyl group of Asp 1 in another peptide. These results show that the active metabolites of the pesticides chlorpyrifos and parathion catalyze the crosslinking of amyloid beta (1-42) into toxic dimers. It was concluded that the increased risk of neurodegenerative disease in people exposed to organophosphorus pesticides could be explained by the crosslinking activity of these chemicals.
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Project description:This is the first study to use a high-throughput metagenomic shotgun approach to explore the biosynthetic potential of soil metagenomes from different pristine environments of northwest Argentina. Our data sets characterize these metagenomes and provide information on the possible effect these ecosystems have on their diversity and biosynthetic potential.
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Project description:In this study, we analyzed the microbial communities from a methane-based bio-reactor with selenate as an electron accepter. Four biological replicates were analyzed by metagenomics, of which data can be found in the SRA database (Accession number: SRP136677, SRP136696, SRP136790 and SRP136859). Based on the metagenomic data, we detected the expressed proteins using metaproteomics. This data is also included in this submission.
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Project description:Pesticides are chemical compounds widely used in agriculture to control pests, since the 1960s. Regardless of its specific targets, such substances, unfortunately, can reach the human organism, and negative cumulative effects have been reported in people worldwide. Chronic exposure to pesticides has been discussed as a significant risk factor for the development of cancer, including breast tumors. Breast cancer is the most common malignant neoplasia that affects women worldwide, whose origin is mostly connected to life habits and the environment, and to a lesser extent to inheritable genetic mechanisms. Therefore, the contribution of substances as pesticides, that are present in the environment continuously, may have a pivotal role in the genesis breast cancer, especially in geographic areas in which women are important players in the rural work and are in direct contact with these compounds. In vitro and experimental studies have broadly reported the mechanisms triggered by pesticides that contribute to breast carcinogenesis, which fall essentially within DNA damage-based events in association with hormones deregulation and rising of metabolites that activate oncogenes (Alleva et al., 2018, BRADLOW et al., 1995). However, few is known about how these mechanisms are connected, as well as the manner that they can correlate with disease prognosis and clinicopathological features in human breast cancer as a result of the toxic consequences of pesticide exposure. In the last years, aiming to expand the knowledge about beyond isolated biological findings, high throughput molecular approaches combined with bioinformatics designs raised as powerful tools to understand breast cancer behavior and biology. Thereby, it was possible to broadcast that breast cancer is a very complex disease, and that distinct mechanisms are activated depending on specific clinicopathological characteristics. As far as we know, there are still no studies reporting the use of proteomics-based strategies to assess the impact of chronic pesticide exposure in women with breast cancer. To fill this gap, the present study proposes a toxicoproteomics perspective to investigate the systemic profile of differentially expressed proteins in the blood of breast cancer patients chronically exposed to pesticides, by using a high-throughput label-free proteomic strategy, and provide an integrative clinicopathological view based on bioinformatics approaches and validation experiments.
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Project description:Exposure to environmental concentrations of organophosphate pesticides in Pacific salmon can cause neurobehavioral injuries leading to loss of survival. However, the molecular mechanisms underlying olfactory impairment remain poorly understood. In the current study, we exposed juvenile salmon to three environmentally-relevant doses of chlorpyrifos (CPF) and malathion (MAL) individually and to three concentrations of binary mixtures of both compounds. Brain acetylcholinesterase (AChE) activity was significantly reduced only in the highest dosage of binary mixture group (47% inhibition). Microarray analysis on RNA from coho olfactory rosettes revealed a number of differentially expressed genes in all exposure groups. Overall, there were little overlapping of affected canonical pathways between CPF groups and MAL groups, suggesting the different biofunctions targeted by these two OP pesticides. Several metabolic and signaling pathways also represented the significant toxicological impact of OP pesticides on olfactory system, such as Aryl Hydrocarbon Receptor Signaling, Xenobiotic Metabolism Signaling, Mitochondrial Dysfunction, Pro-Apoptosis, and Oxidative Stress.
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