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5,596 results for “Epigenetics”
Grandmaternal allergen sensitization reprograms epigenetic and airway responses to allergen in second generation offspring
<p><strong>SUPPLEMENTARY FIGURE LEGEND</strong></p> <p><strong>Supplemental Figure 1. Grandmaternal allergen sensitization during pregnancy regulates differentially methylated cytosines in airway epithelium of second-generation offspring at baseline and after allergen sensitization</strong>. Grandmaternal HDM exposure resulted in 1,390 DMCs in airway epithelium of F2 offspring at baseline (F0 HDM•F2 Base vs F0 Veh•F2 Base). F2 HDM sensitization alone resulted in 1,467 DMCs (F0Veh•F2Sens vs F0 Veh•F2 Base). In contrast, HDM sensitization in F2 mice from HDM-exposed founders resulted in 3,756 total DMCs (F0 HDM•F2 Sens vs F0 HDM•F2 Base). N=8 total for each group (n=4 males and n=4 females).</p> <p> </p> <p><strong>Supplemental Figure 2. Gene ontology analysis of DMCs in airway epithelium of second-generation offspring</strong>. Gene ontology analysis of DMCs in airway epithelium of F2 mice identified enriched biological processes (individual small circles), which were then grouped based on functional annotation using Cytoscape Enrichment Map (larger, labeled, black circles). Each small circle represents an individual biological process and size is proportional to number of involved genes, while connecting edges represent shared genes between individual biological processes. (A) Gene ontology analysis showing enriched biological processes due to grandmaternal HDM exposure in F2 offspring at baseline (F0 HDM•F2 Base versus F0 VEH•F2 Base). (B) Gene ontology analysis showing effects of HDM sensitization alone on enriched biological processes in F2 offspring from vehicle-exposed F0 mice (F0 Veh•F2 Sens vs F0 VEH•F2 Base). (C) Gene ontology analysis showing potentiating effects of F0 grandmaternal HDM exposure on enriched biological processes after HDM sensitization in F2 mice (F0 HDM•F2 Sens vs F0 HDM•F2 Base). N=8 total for each group (n=4 males and n=4 females).</p> <p> </p> <p><strong>Supplementary Figure 3. Differential methylation is linked to altered gene expression in airway epithelium of second-generation offspring. </strong>A subset of F2 airway epithelial genes identified during differentially-methylated pathway analyses were analyzed by real-time RT-PCR to assess for expression. Grandmaternal HDM exposure significantly increased Smad3 expression at baseline and potentiated its response after F2 HDM sensitization. Paxillin expression was also increased after HDM sensitization compared to non-sensitized F2 descendants from HDM exposed founders, although this difference did not meet statistical significance (<em>p</em> = 0.06). No differences were observed between Ets3, Cdh3, or Cacna1d expression between groups. *<em>p</em> < 0.05. Delta CT values were analyzed with two-way ANOVA and Tukey’s post-test. N=8 total for each group (n=4 males “open circles” and n=4 females “closed circles”), except for F0 HDM•F2 Base, n=5.</p> <p> </p> <p><strong>Supplementary Figure 4. Grandmaternal allergen exposure during pregnancy regulates vagal ganglia cytosine methylation in second-generation offspring at baseline and after allergen sensitization</strong>. Grandmaternal HDM sensitization during pregnancy resulted in 901 DMCs in F2 mice at baseline (F0 HDM•F2 Base vs F0 Veh•F2 Base). F2 HDM sensitization alone resulted in 1,467 DMCs (F0Veh•F2Sens vs F0 Veh•F2 Base). In contrast, HDM sensitization in F2 mice from HDM-sensitized F0 grandmaternal founders resulted in 1,787 total DMCs (F0 HDM•F2 Sens vs F0 HDM•F2 Base). N=8 total for each group (n=4 males and n=4 females).</p> <p> </p> <p><strong>Supplementary Figure 5. Grandmaternal allergen sensitization during pregnancy modifies epigenetic signatures in second-generation offspring in a tissue-specific manner. </strong>Only rarely were differentially methylated genes shared between vagal ganglia neurons and airway epithelium in all groups. Specifically, neurons and epithelium in non-sensitized F2 mice from grandmaternal HDM-sensitized F0 founders shared only 15 genes in common (light blue circles). Neurons and epithelium in HDM-sensitized F2 mice from Vehicle-exposed grandmaternal founders shared only 9 genes in common (grey circles). Neurons and epithelium in HDM-sensitized F2 mice from HDM-sensitized grandmaternal F0 founders shared only 41 genes in common. N=8 total for each group (n=4 males and n=4 females).</p> <p> </p> <p><strong>Supplementary Figure 6. Gene ontology analysis of biological process enrichment in vagal ganglia from second-generation offspring</strong>. Gene ontology analysis of DMCs in vagal ganglia of F2 mice identified enriched biological processes (individual small circles), which were then grouped based on functional annotation using Cytoscape Enrichment Map (larger, labeled, black circles). Each small circle represents an individual biological process and size is proportional to number of involved genes, while connecting edges represent shared genes between individual biological processes. (A) Gene ontology analysis showing effects of HDM sensitization on biological process enrichment in F2 offspring from vehicle-exposed F0 mice (F0 Veh•F2 Sens vs F0 VEH•F2 Base). (B) Gene ontology analysis showing potentiating effects of F0 grandmaternal HDM sensitization on biological process enrichment in F2 mice after HDM sensitization (F0 HDM•F2 Sens vs F0 HDM•F2 Base). N=8 total for each group (n=4 males and n=4 females).</p> <p> </p> <p><strong>Supplemental Figure 7. Quantification of airway sensory nerve density using 3D confocal microscopy.</strong> Airway epithelial substance P-positive sensory nerves were analyzed in whole mount specimens using immunofluorescence and 3-dimensional confocal microscopy. Total nerve length and the number of branch points were quantified from nerve models generated based on substance P-positive voxels. Top) Representative images of substance P-expressing nerves (purple, top left) and nerve modeling (white filaments, top right). Bottom) Nerve length (left) and the number of branch points (right) were similar between untreated F2 mice from HDM exposed grandmothers and vehicle exposed grandmothers. N=6 both groups (n=3 males “open circles” and n=3 females “closed circles”).</p> <p> </p> <p><strong>SUPPLEMENTAL TABLES</strong></p> <p><strong>Supplemental Table S1.</strong> Pathways identified by DMC analysis that were not present on DMR analysis in airway epithelium of second-generation F2 mice. All DMR-associated pathways were also identified by DMC analysis, as indicated in Table 1 in main text.</p> <p> </p> <p><strong>Supplemental Table S2. </strong>Over-represented transcription factor binding sites in DMRs of airway epithelium and vagal ganglia from F2 mice before and after allergen sensitization.</p> <p> </p> <p><strong>Supplemental Table S3. </strong>Pathway identified by DMC analysis in vagal ganglia of second-generation F2 mice. All DMR-associated pathways were also identified by DMC analysis, as indicated in Table 3 in main text.</p> <p> </p> <p><strong>SUPPLEMENTARY DATA FILES</strong></p> <p><strong>Lebold&Cook_DMC_Gene List.xlsx. </strong></p> <p><strong>Lebold&Cook_DMR Gene List.xlsx.</strong></p> <p>Differentially methylated cytosines (DMC) and regions (DMR) source data files.</p>
DNA methylation-based age prediction and sex-specific epigenetic aging in a lizard with female-biased longevity
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Mitochondrial epigenetics brings new perspectives on doubly uniparental inheritance in bivalves
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Pollution induces epigenetic effects that are stably transmitted across multiple generations
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Epigenetic aging of Māui and Hector's dolphins
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Designing epigenetic clocks for wildlife research
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Independent avian epigenetic clocks for aging and development
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Data from: Environmental enrichment induces intergenerational behavioural and epigenetic effects on fish
Parental effects influence offspring phenotypes through pre- and post-natal routes but little is known about their molecular basis, and therefore their adaptive significance. Epigenetic modifications, which control gene expression without changes in the DNA sequence and are influenced by the environment, may contribute to parental effects. We investigated the effects of environmental enrichment on the behaviour, metabolic rate and brain DNA methylation patterns of parents and offspring of the highly inbreed mangrove killifish (Kryptolebias marmoratus). Parental fish reared in enriched environments had lower cortisol levels, lower metabolic rates and were more active and neophobic than those reared in barren environments. They also differed in 1,854 methylated cytosines (DMCs). Offspring activity and neophobia were determined by the parental environment. Among the DMCs of the parents, 98 followed the same methylation patterns in the offspring, three of which were significantly influenced by parental environments irrespective of their own rearing environment. Our results suggest that parental environment influences the behaviour and, to some extent, the brain DNA methylation patterns of the offspring.
Endocrine disruptors cause multigenerational and transgenerational epigenetic changes in fish exposed during early life
<p>The inland silverside, <i>Menidia beryllina</i>, is a euryhaline fish and a model organism in ecotoxicology. We previously showed that exposure to picomolar (ng/L) levels of endocrine disrupting chemicals (EDCs) can cause a variety of effects in <i>M. beryllina</i>, from changes in gene expression to phenotypic alterations. Here we explore the potential for early life exposure to EDCs to modify the epigenome in silversides, with a focus on multi- and transgenerational effects. EDCs included contaminants of emerging concern (the pyrethroid insecticide bifenthrin and the synthetic progestin levonorgestrel), as well as a commonly detected synthetic estrogen (ethinylestradiol), and a synthetic androgen (trenbolone) at exposure levels ranging from 3 to 10 ng/L. In a multigenerational experiment, we exposed parental silversides to EDCs from fertilization until 21 days post hatch (dph). Then we assessed DNA methylation patterns for three generations (F0, F1, and F2) in whole body larval fish using reduced representation bisulfite sequencing (RRBS). We found significant ( = 0.05) differences in promoter and/or gene body methylation in treatment fish relative to controls for all EDCs and all generations indicating that both multigenerational (F1) and transgenerational (F2) effects that were caused by strict inheritance of DNA methylation alterations and the dysregulation of epigenetic control mechanisms. Using gene ontology and pathway analyses, we found enrichment in biological processes and pathways representative of growth and development, immune function, reproduction, pigmentation, epigenetic regulation, stress response and repair (including pathways important in carcinogenesis). Further, we found that a subset of potentially EDC responsive genes (EDCRGs) were differentially methylated across all treatments and generations and included hormone receptors, genes involved in steroidogenesis, prostaglandin synthesis, sexual development, DNA methylation, protein metabolism and synthesis, cell signaling, and neurodevelopment. The analysis of EDCRGs provided additional evidence that differential methylation is inherited by the offspring of EDC-treated animals, sometimes in the F2 generation that was never exposed. These findings show that low, environmentally relevant levels of EDCs can cause altered methylation in genes that are functionally relevant to impaired phenotypes documented in EDC-exposed animals and EDC exposure has the potential to affect epigenetic regulation in fish that have not been directly exposed.</p>
Epigenetic Profiling of Social Communication Trajectories and Co-occurring Mental Health Problems: A Prospective, Methylome-wide Association Study
<p>While previous studies suggest that both genetic and environmental factors play an important role in the development of autism-related traits, little is known about potential biological mechanisms underlying these associations. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we examined prospective associations between DNA methylation (DNAm: N-birth=804, N-age7=877) and trajectories of social communication deficits (8-17 years). Methylomic variation at three loci across the genome (false discovery rate=0.048) differentiated children following high (n=80) versus low (n=724) trajectories of social communication deficits. This differential DNAm was specific to the neonatal period and not observed at age 7. Associations between DNAm and trajectory membership remained robust after controlling for co-occurring mental health problems (i.e., hyperactivity/inattention, conduct problems). The three loci identified at birth were not replicated in the Generation R Study. However, to the best of our knowledge, ALSPAC is the only study to date that is prospective enough to examine DNAm in relation to longitudinal trajectories of social communication deficits from late childhood to late adolescence. Although the present findings might point to potentially novel sites that differentiate between a high versus low trajectory of social communication deficits, the results should be considered tentative until further replicated.</p> <p>This dataset contains summary statistics for the methylome-wide association study using DNAm data collected from individuals at birth.</p> <p>Upload of this dataset was completed by The EWAS Catalog team. The data can be queried along with hundreds of other EWAS at ewascatalog.org. To upload your EWAS summary statistics and have a zenodo DOI generated for you go to ewascatalog.org/upload</p>
Data from: Genetic responsiveness of African buffalo to environmental stressors: a role for epigenetics in balancing autosomal and sex chromosome interactions?
In the African buffalo (Syncerus caffer) population of the Kruger National Park (South Africa) a primary sex-ratio distorter and a primary sex-ratio suppressor have been shown to occur on the Y chromosome. A subsequent autosomal microsatellite study indicated that two types of deleterious alleles with a negative effect on male body condition, but a positive effect on relative fitness when averaged across sexes and generations, occur genome-wide and at high frequencies in the same population. One type negatively affects body condition of both sexes, while the other acts antagonistically: it negatively affects male but positively affects female body condition. Here we show that high frequencies of male-deleterious alleles are attributable to Y-chromosomal distorter-suppressor pair activity and that these alleles are suppressed in individuals born after three dry pre-birth years, likely through epigenetic modification. Epigenetic suppression was indicated by statistical interactions between pre-birth rainfall, a proxy for parental body condition, and the phenotypic effect of homozygosity/heterozygosity status of microsatellites linked to male-deleterious alleles, while a role for the Y-chromosomal distorter-suppressor pair was indicated by between-sex genetic differences among pre-dispersal calves. We argue that suppression of male-deleterious alleles results in negative frequency-dependent selection of the Y distorter and suppressor; a prerequisite for a stable polymorphism of the Y distorter-suppressor pair. The Y distorter seems to be responsible for positive selection of male-deleterious alleles during resource-rich periods and the Y suppressor for positive selection of these alleles during resource-poor periods. Male-deleterious alleles were also associated with susceptibility to bovine tuberculosis, indicating that Kruger buffalo are sensitive to stressors such as diseases and droughts. We anticipate that future genetic studies on African buffalo will provide important new insights into gene fitness and epigenetic modification in the context of sex-ratio distortion and infectious disease dynamics.
Epigenetic aging signatures in mice livers are slowed by dwarfism, calorie restriction and rapamycin treatment
<p>Processed dataset and source data for iPython notebooks hosted by: https://doi.org/10.5281/zenodo.291961</p>
Aracena et al- Epigenetic variation impacts individual differences in the transcriptional response to influenza infection
<p>-Inputs for Github code</p><p>-Full methylation results</p><p>-Full QTL results</p>
A distinct isoform of lymphoid enhancer binding factor 1 (LEF1) epigenetically restricts EBV reactivation to maintain viral latency
<p>As a human tumor virus, EBV is present as a latent infection in its associated malignancies where genetic and epigenetic changes have been shown to impede cellular differentiation and viral reactivation. We reported previously that levels of the Wnt signaling effector, lymphoid enhancer binding factor 1 (LEF1) increased following EBV epithelial infection and an epigenetic reprogramming event was maintained even after loss of the viral genome. Elevated LEF1 levels are also observed in nasopharyngeal carcinoma and Burkitt lymphoma. To determine the role played by LEF1 in the EBV life cycle, we used in silico analysis of EBV type 1 and 2 genomes to identify over 20 Wnt-response elements, which suggests that LEF1 may bind directly to the EBV genome and regulate the viral life cycle. Using CUT&RUN-seq, LEF1 was shown to bind the latent EBV genome at various sites encoding viral lytic products that included the immediate early transactivator BZLF1 and viral primase BSLF1 genes. The LEF1 gene encodes various long and short protein isoforms. siRNA depletion of specific LEF1 isoforms revealed that the alternative-promoter derived isoform with an N-terminal truncation (∆N LEF1) transcriptionally repressed lytic genes associated with LEF1 binding. In addition, forced expression of the ∆N LEF1 isoform antagonized EBV reactivation. As LEF1 repression requires histone deacetylase activity through either recruitment of or direct intrinsic histone deacetylase activity, siRNA depletion of LEF1 resulted in increased histone 3 lysine 9 and lysine 27 acetylation at LEF1 binding sites and across the EBV genome. Taken together, these results indicate a novel role for LEF1 in maintaining EBV latency and restriction viral reactivation via repressive chromatin remodeling of critical lytic cycle factors.</p>
Overcoming clinical resistance to EZH2 inhibition using rational epigenetic combination therapy
<p>Supplementary data for Kazansky et al, "Overcoming clinical resistance to EZH2 inhibition using rational epigenetic combination therapy" and "Epigenetic targeting of PGBD5-dependent DNA damage in SMARCB1-deficient sarcomas." Raw RNA-seq data from G401 cells can be found at the Gene Expression Omnibus (GEO) repository, accession number GSE213845. RNA-seq data from patient tumor samples has been deposited to the Database of Genotypes and Phenotypes (dbGaP), accession number phs003188.v1.p1.</p> <p>All files are labeled with their corresponding figures.</p> <p>"DESeq_processing_FINAL.R" was used for analysis of patient RNA-seq data, using "20230131_SampleTable.csv" and all "*_htseq.txt" files as input.</p> <p>"Tumor_growth_analysis_FINAL_UPDATED" was used for analysis of tumor growth kinetics using the aucVardiTest function. This was used for both of the manuscripts desscribed above.</p>
Multimodal Epigenetic Sequencing Analysis (MESA) of Cell-free DNA for Non-invasive Colorectal Cancer Detection
<p>Processed data (feature-by-sample matrices) of non-disruptive bisulfite-free methylation sequencing for cfDNA samples from 4 clinical cohorts (Cohort 1, Cohort 2, Cohort 3, and cfTAPS dataset). Codes used to repeat the results in our paper can be found https://rpubs.com/LiYumei/926228 and https://github.com/ChaorongC/MESA. </p>
Multi-omics analysis of innate and adaptive responses to BCG vaccination reveals epigenetic cell states that predict trained immunity
<p>This repository contains personal immune profiles of 323 healthy individuals (300BCG) subjected to Bacillus Calmette-Guérin (BCG) with blood samples collected immediately before (day 0), and 14 and 90 days after the vaccination. The personal immune profiles comprise:</p> <ul> <li>immune cell concentrations measured with flow cytometry and a hematology analyzer</li> <li>plasma concentrations of 73 circulating inflammatory markers</li> <li>30 measurements of cytokine and lactate production capacity of peripheral blood mononuclear cells (PBMCs) in response to four microbial stimuli (Candida albicans, Escherichia coli lipopolysaccharide [LPS], Staphylococcus aureus, Mycobacterium tuberculosis).</li> </ul> <p>Visit <a href="http://300BCG.bocklab.org/">http://300BCG.bocklab.org/</a> to learn more.</p>
Supplementary Data for "Epigenetic mechanisms controlling human leukemia stem cells and therapy resistance"
<p><strong>We performed functional genomic profiling of diverse leukemias using label tracing techniques. We identified AML stem cell quiescence is defined by distinct promoter-centered chromatin and gene expression dynamics, and controlled by a novel transcription factor network, which is associated with disease persistence and chemotherapy resistance in multiple patients. </strong></p>
Genome-wide DNA methylation profiling identifies epigenetic signatures of β-lactams induced fatal anaphylactic shock
<p>Drug hypersensitivity is one of the most frequent causes of anaphylaxis in adults, of which antibiotics are the most common culprits, particularly β-lactams induced anaphylactic shock deaths. We provided the genome wide DNA methylation profiling study of PBMC from 14 individuals peripheral venous blood samples. Illumina Infinium Human Methylation EPIC BeadChip was used. Among the 14 individuals, 8 patients were died from β-lactams induced anaphylactic shock, 6 healthy individuals were controls. Inclusion criteria for the β-lactams induced anaphylactic shock as follows: ①A clear history of β-lactams transfusion or components of β-lactams detected from blood (or skin of suspicious infusion site); ②Shock symptoms occurred after infusion of β-lactams and died within a short period of time; ③The immunohistochemical results of throat, lung and gastrointestinal tissues showed that tryptase or chymase were mostly positive expression; ④ Excluding other causes (disease, poisoning) of death; ⑤ No decay occurred in the corpse.Inclusion criteria for controls as follows: ① Healthy, no previous common underlying diseases and no history of genetic disease; ② No history of allergies to drugs, food, pollen and so on; ③Skin prick test (SPT) is negative, allergen-specific IgE (sIgE)< 100IU/mL; the skin test results of β-lactam drugs were negative.</p>
Genetic and epigenetic differentiation across intertidal gradients in the foundation plant Spartina alterniflora
<p>This record contains supplementary information for the article "Genetic and epigenetic differentiation across intertidal gradients in the foundation plant Spartina alterniflora". It contains the barcodes (barcodes.txt), the reference contigs (contigs.fasta.gz), the annotation of the reference contigs (mergedAnnot.csv.gz), the SNPs (snps.vcf.gz), the methylation data (methylation.txt.gz), and the experimental design (design.txt). All data are unfiltered.</p> <p>All reads are available on SRA (PRJNA798549). Note that the barcode sequences and the control nucleotide were already removed from the demultiplexed files (hence, for each sample, reads are also split into "watson" and "crick" based on the control nucleotide).</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.