Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GNPS - Leaf metabolic signatures induced by real and simulated herbivory in black mustard (Brassica nigra)

ABSTRACT: LC-TOF-MS analysis of black mustard leaves exposed to methyl-jasmonate and caterpillar herbivory by Pieris brassicae. Metabolites: glucosinolates, phenylpropanoids (sinapic acid derivatives, and flavonol glucosides).

INSTRUMENT(S): ACQUITY UPLC

ORGANISM(S): Brassica Nigra (ncbitaxon:3710)

SUBMITTER: Benedicte Albrectsen

PROVIDER: MSV000084183 | GNPS | Thu Aug 08 10:14:00 BST 2019

REPOSITORIES: GNPS

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Metabolic signatures induced by real and simulated herbivory in black mustard (Brassica nigra)

Project description:LC-TOF-MS analysis of black mustard leaves exposed to methyl-jasmonate and caterpillar herbivory by Pieris brassicae. Metabolites: glucosinolates, phenylpropanoids (sinapic acid derivatives, and flavonol glucosides).

2019-08-08 | MSV000084183 | MassIVE

Leaf metabolic signatures induced by real and simulated herbivory in black mustard (Brassica nigra).

Project description:INTRODUCTION:The oxylipin methyl jasmonate (MeJA) is a plant hormone active in response signalling and defence against herbivores. Although MeJA is applied experimentally to mimic herbivory and induce plant defences, its downstream effects on the plant metabolome are largely uncharacterized, especially in the context of primary growth and tissue-specificity of the response. OBJECTIVES:We investigated the effects of MeJA-simulated and real caterpillar herbivory on the foliar metabolome of the wild plant Brassica nigra and monitored the herbivore-induced responses in relation to leaf ontogeny. METHODS:As single or multiple herbivory treatments, MeJA- and mock-sprayed plants were consecutively exposed to caterpillars or left untreated. Gas chromatography (GC) and liquid chromatography (LC) time-of-flight mass-spectrometry (TOF-MS) were combined to analyse foliar compounds, including central primary and specialized defensive plant metabolites. RESULTS:Plant responses were stronger in young leaves, which simultaneously induced higher chlorophyll levels. Both MeJA and caterpillar herbivory induced similar, but not identical, accumulation of tricarboxylic acids (TCAs), glucosinolates (GSLs) and phenylpropanoids (PPs), but only caterpillar feeding led to depletion of amino acids. MeJA followed by caterpillars caused higher induction of defence compounds, including a three-fold increase in the major defence compound allyl-GSL (sinigrin). When feeding on MeJA-treated plants, caterpillars gained less weight indicative of the reduced host-plant quality and enhanced resistance. CONCLUSIONS:The metabolomics approach showed that plant responses induced by herbivory extend beyond the regulation of defence metabolism and are tightly modulated throughout leaf development. This leads to a new understanding of the plant metabolic potential that can be exploited for future plant protection strategies.

| S-EPMC6765471 | biostudies-literature

Hepatic gene expression in C57BL/6 mice intratracheally instilled with Printex 90 carbon black nanoparticles

2012-04-13 | GSE35192 | GEO

Transcriptomic profiling of human induced pluripotent stem cells derived cardiomyocytes (hiPSC-CMs) and cardiac progentiors (hiPSC-CPs) from tetralogy of Fallot (TOF) patients with DiGeorge Syndrome (DG) and without DiGeorge Syndrome (ND)

Project description:DG accounts for most of the identifiable cases of TOF. Exploring and comparing the transcriptome of hiPSC-CMs and hiPSC-CPs from TOF-DG and TOF-ND could provide a bettering understanding on TOF.

2023-08-29 | GSE186293 | GEO

Transcriptome analysis defines ToF and ASD myocardial gene signatures and reveals disease-specific gene reprogramming upon surgery with cardiopulmonary bypass

Project description:Tetralogy of Fallot (ToF) and Atrial Septal Defects (ASD) are the most common types of congenital heart disease and a major cause of childhood morbidity and mortality. Cardiopulmonary bypass (CPB) is used during corrective cardiac surgery to support circulation and heart stabilization. However, this technique triggers systemic inflammatory and stress response and consequent increased risk of postoperative complications. The aim of this study was to define the molecular bases of ToF and ASD pathogenesis and response to CPB and identify new specific biomarkers. We conducted comparative transcriptome analysis of right atrial biopsies from 10 ToF and 10 ASD patients before (Pre-CPB) and after (Post-CPB) surgery. Pre-CPB samples showed significant differential expression of 72 genes (DEGs), 28 of which were overexpressed in ToF and 44 in ASD. According to Gene Ontology annotation, the mostly enriched biological processes were represented by matrix organization and cell adhesion in ToF and by muscle development and contractility in ASD specimens. GSEA highlighted the specific enrichment of known hypoxia gene sets in ToF samples, pointing to a role for hypoxia in disease pathogenesis. The post-CPB myocardium exhibited significant alterations in the expression profile of genes related to transcription regulation, growth/apoptosis, inflammation, cell adhesion/matrix organization, and oxidative stress. Among DEGs, only 70 were common to the two disease groups, whereas 110 and 24 were unique in ToF and ASD, respectively. Interestingly, gene expression changes in ASD samples followed a consensus hypoxia profile. These data define ToF- and ASD-specific myocardial transcriptional signatures and demonstrate differential gene reprogramming in response to CPB in the two pathologies, with potential prognostic and therapeutic implications.

2020-01-21 | GSE132176 | GEO

Hepatic gene expression in C57BL/6 mice intratracheally instilled with Printex 90 carbon black nanoparticles

Project description:We investigated hepatic mRNA profiles of female mice exposed to 0.162 mg Printex 90 carbon black nanoparticles by single intra-tracheal instillation. We examined responses to this dose 1, 3 and 28 days after exposure, alongside respective controls. We show that genes part of the 3-hydroxy-3-methyl-glutaryl-CoA reductase pathway to be up-regulated by exposure to Printex 90. individual total RNA (200 ng) from 6 mice per treatment group (control and 0.162mg) and universal reference total RNA (Stratagene, Mississauga, ON, Canada) was used to synthesize double stranded cDNA.

2012-04-12 | E-GEOD-35192 | biostudies-arrayexpress

Comparative DNA methylation and gene expression analysis identifies novel genes for structural congenital heart diseases

Project description:The most common congenital heart disease (CHD) is the ventricular septal defect (VSD), which is also a subfeature of Tetralogy of Fallot (TOF) representing the most common form of cyanotic CHD. The underlying causes for the majority of CHDs are still unclear and most probably consist of combinations of genetic, epigenetic and environmental factors. DNA methylation is the most widely studied epigenetic modification and several cardiac regulators have already been shown to be differentially methylated in CHD patients. Here, we present the first analysis of genome-wide DNA methylation data obtained from cardiac biopsies of TOF and VSD patients. We applied affinity-based enrichment of methylated DNA sequences with methyl-CpG-binding domain proteins followed by next-generation sequencing (MBD-Seq). MBD-seq on cardiac biopsies of patients with Tetralogy of Fallot and ventricular septal defect

2016-08-08 | E-GEOD-62629 | biostudies-arrayexpress

Comparative DNA methylation and gene expression analysis identifies novel genes for structural congenital heart diseases

2016-08-08 | GSE62629 | GEO

Alkylation-induced gene expression changes in Aag knock-out liver

Project description:We catalogued and quantified the transcripts in livers of wild-type and Aag-deficient mice that had been exposed to the model alkylating agent methyl methanesulfonate (MMS). Gene expression analysis was performed for samples harvested 6 hours post-MMS treatment.

2018-06-04 | GSE115254 | GEO

Network exploration of gene signatures underlying low birth weight induced metabolic alterations.

Project description:BackgroundThis study explored underlying gene signatures of low birth weight (LBW) by analyzing differentially expressed genes (DEGs) between LBW and normal birth weight (NBW) subjects.MethodsSubjects with different birth weight was collected from GEO database. P < .05 and | logFC | ≥ 1.0 were used for screening DEGs. David (2021 Update) was used to perform GO annotation and KEGG signaling pathway enrichment analysis. The protein-protein interaction network of DEGs was constructed using the STRING database, in which hub genes were mined through Cytoscape software.ResultsA total of 326 DEGs were identified, including 287 up-regulated genes and 39 down-regulated genes. The GO biological processes enriched by DEGs mainly involved epidermal growth, keratinization and intermediate fibrous tissue. The DEGs were significantly enriched in intracellular insoluble membranes, desmosomes and extracellular space. Their molecular functions mainly focused on structural molecular activity, structural components of epidermis and structural components of cytoskeleton. PI3K/AKT signaling pathway and tight junction were highlighted as critical pathways enriched by DEGs. Ten hub genes which included KRT14, EGF, DSP, DSG1, KRT16, KRT6A, EPCAM, SPRR1B, PKP1, and PPL were identified from the constructed protein-protein interaction network.ConclusionA total of 326 DEGs and 10 hub genes were identified as candidates for metabolic disorders in LBW individuals. Our results indicated PI3K/AKT signaling pathway as an intrauterine adaptive mechanism for LBW individuals. We observed activated PI3K/AKT pathway in LBW individuals, which would promote growth and development at the early stage of life, but adversely introduce extra metabolic stress and thereby potentially induce metabolic disorders in adulthood.

| S-EPMC9622720 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data