Journal: BMC Plant Biology

Article Title: Insights into epigenetics suggest a role of DNA methylation in regulating Chinese yam tuber shape

doi: 10.1186/s12870-026-08438-5

Figure Lengend Snippet: Whole-genome DNA methylation analysis of Chinese yam variant F2000 and F60. A Principal component 1 and principal component 2 analyses were performed for each sample. B Methylation level distribution across genetic features including 4 kb upstream of TSS, gene body, and 4 kb downstream of TTS in the three DNA methylation contexts CG, CHG, and CHH. Analyses were performed in biological triplicates for each variant. C Number of DMRs with higher methylation levels in F2000 (hypermethylated) and in F60 (hypomethylated). DMRs were investigated in the three DNA methylation contexts CG, CHG and CHH. Distribution of DMRs upstream in the putative promoter (4 kb of TSS), within the gene body, and down-stream in the putative terminator (4 kb of TTS) were analyzed in DMR-associated genes (q-value ≤ 0.01, methylation difference >|10%|). D Venn analysis of DMR-associated genes split in hyper- and hypomethylated promoters, gene bodies, and terminators. DMR, differentially methylated region; TSS, transcription start site; TTS, transcription termination site

Article Snippet: Prepared DNA samples were sent to Novogene Company (Beijing, China) for low-input whole-genome bisulfite sequencing including the steps of bisulfite treatment and library construction.

Techniques: DNA Methylation Assay, Variant Assay, Methylation

Journal: Cells

Article Title: Pre-Conception Maternal Obesity Confers Autism Spectrum Disorder-like Behaviors in Mice Offspring Through Neuroepigenetic Dysregulation

doi: 10.3390/cells14151201

Figure Lengend Snippet: Experimental design. ( A ) Schematic representation of the experimental design. Three main groups were generated using IVF and two-cell-stage embryo transfer. Oocytes from either high fat diet (HFD)-fed or normal diet (ND)-fed female C57BL/6J mice were fertilized in vitro with sperm from ND-fed C57BL/6J males. Resulting two-cell embryos were transferred into pseudopregnant CD-1 surrogate females fed either the ND or HFD. Offspring were delivered naturally and cross-fostered at birth by ND-fed CD-1 dams to standardize postnatal maternal care. ( B ) Group stratification used for downstream analyses. Three IVF-derived experimental groups were defined by the gamete donor and surrogate environment. Behavioral phenotyping was used to classify male offspring into the ASD or unaffected subgroups. From the GAM-HFD group, male offspring were further stratified as either ASD (affected) or NESTED (unaffected) based on behavioral outcomes. ( C ) Behavioral testing schedule. A battery of ASD-relevant behavioral assays was conducted: USV on PND 8, 10, and 12; the three-chamber test for social interaction on PND 25; the self-grooming test for repetitive behavior on PND 30; and the elevated plus maze test for anxiety-like behavior on PND 40. Tests were spaced by at least 24 h to minimize stress. ( D ) Molecular analyses were performed on PND 41. Cortical tissue was used for mRNA expression and alternative splicing analysis via RNA-Seq; hippocampal tissue was used for genome-wide DNA methylation profiling using WGBS. Analyses were performed on three representative male animals per group (CONTROL, NESTED, and ASD). Created with Biorender.com (Science Suite Inc., Toronto, ON, Canada).

Article Snippet: Whole-genome bisulfite sequencing (WGBS) was conducted by Macrogen Inc. on 250 ng of hippocampal DNA from each sample.

Techniques: Generated, In Vitro, Derivative Assay, Battery, Expressing, Alternative Splicing, RNA Sequencing, Genome Wide, DNA Methylation Assay, Control

Journal: Cells

Article Title: Pre-Conception Maternal Obesity Confers Autism Spectrum Disorder-like Behaviors in Mice Offspring Through Neuroepigenetic Dysregulation

doi: 10.3390/cells14151201

Figure Lengend Snippet: Differential DNA methylation at an alternative promoter of Homer1 correlates with isoform-specific expression. Significant group-specific differences in DNA methylation were observed within the promoter and exon 1 region of Homer1 , a locus associated with synaptic scaffolding and plasticity. Two distinct promoter regions were identified: the canonical promoter (5′) and an alternative downstream promoter overlapping a CpG island and a cis -regulatory element (CRE). While no significant differences were found in methylation at the canonical promoter across groups (Kruskal–Wallis test, χ 2 = 0.96, p = 0.618; mean methylation: CONTROL = 6.17%, ASD = 4.83%, NESTED = 4.0%), the alternative promoter showed marked hypomethylation in the ASD group. Specifically, the alternative promoter was hypermethylated in the CONTROL group and one NESTED sample, but completely unmethylated in ASD mice (Fisher’s exact test, p = 0.01). This regional hypomethylation corresponded with increased expression of Homer1a , the short, activity-inducible isoform, in ASD offspring (mean RPKM: ASD = 2800 ± 280 vs. CONTROL = 200 ± 50; unpaired two-tailed t -test, p = 0.001). While the WGBS and RNA-Seq data were derived from distinct brain regions (hippocampus and cortex, respectively), the observed pattern suggests a potentially conserved epigenetic regulatory mechanism. However, we note that this correlation is indirect given the different tissue types evaluated. Equally scaled tracks show the percentage of DNA methylation (top) and normalized RNA expression (RPKM, bottom) across individual samples for each group (GAM-HFD, NESTED, and CONTROL). The genome architecture includes annotated cis -regulatory elements, the CpG island, and exon 1. The base-level nucleotide positions of the analyzed CRE-containing CpGs are displayed below.

Article Snippet: Whole-genome bisulfite sequencing (WGBS) was conducted by Macrogen Inc. on 250 ng of hippocampal DNA from each sample.

Techniques: DNA Methylation Assay, Expressing, Scaffolding, Methylation, Control, Activity Assay, Two Tailed Test, RNA Sequencing, Derivative Assay, RNA Expression

Journal: bioRxiv

Article Title: TIGAR DEFICIENCY ENHANCES CARDIAC RESILIENCE THROUGH EPIGENETIC PROGRAMMING OF PARKIN EXPRESSION

doi: 10.1101/2025.07.14.664830

Figure Lengend Snippet: A-C, Echocardiograms and quantification of left ventricular ejection fraction (EF), mass (LVM), and end-diastolic volume (LVEDV) in 4-month-old male WT (n=10) and TKO mice (n=13) 4 weeks after myocardial infarction (MI). MI was induced by left anterior descending (LAD) artery ligation. Sham-operated mice served as controls. D-F, Echocardiograms and quantification of left ventricular ejection fraction (EF), mass (LVM), and end-diastolic volume (LVEDV) in 4-month-old male control Myh6Cre mice (n=6) and hTKO mice (n=4) 4 weeks after MI. G-H, RNA-seq analysis of mitochondrial-encoded genes (G) and nuclear-encoded mitochondrial genes (H) from the infarct zone, expressed as fold changes in TKO vs WT. I, Immunoblot analysis of TIGAR, Troponin I, SERCA2, α-actinin1, and Vinculin in infarcted heart tissue from WT and TKO mice, with normal left ventricular tissue (Control LV) as reference. J, RNA-seq analysis of cardiac marker genes from the infarct zone, expressed as fold changes in TKO vs WT. For RNA-seq analyses (G, H, J), RNA from 3 mice per group was pooled for sequencing. Data represent mean±SD; *P<0.05.

Article Snippet: These samples were submitted to Novogene for whole genome bisulfite sequencing, library preparation, and sequencing using their established protocols.

Techniques: Ligation, Control, RNA Sequencing, Western Blot, Marker, Sequencing

Journal: bioRxiv

Article Title: TIGAR DEFICIENCY ENHANCES CARDIAC RESILIENCE THROUGH EPIGENETIC PROGRAMMING OF PARKIN EXPRESSION

doi: 10.1101/2025.07.14.664830

Figure Lengend Snippet: Representative immunofluorescence images of heart sections from WT and TKO mice showing sham myocardium, non-infarct myocardium, and infarct myocardium. Sections were stained for DAPI (blue, nuclei), α-actinin (green, cardiomyocytes), and periostin (red, fibrosis marker). B, RNA sequencing analysis of fibrosis marker genes Postn (periostin) and Lgals3 (galectin-3) in left ventricle (LV), infarct zone, border zone, and remote zone of WT and TKO hearts. TKO hearts demonstrated reduced expression of fibrosis markers in non-infarct (remote) myocardium compared with WT hearts.

Article Snippet: These samples were submitted to Novogene for whole genome bisulfite sequencing, library preparation, and sequencing using their established protocols.

Techniques: Immunofluorescence, Staining, Marker, RNA Sequencing, Expressing

Journal: bioRxiv

Article Title: TIGAR DEFICIENCY ENHANCES CARDIAC RESILIENCE THROUGH EPIGENETIC PROGRAMMING OF PARKIN EXPRESSION

doi: 10.1101/2025.07.14.664830

Figure Lengend Snippet: RNA sequencing analysis comparing gene expression ratios (TKO-Infarct/WT-Infarct) in infarct zones. A, Ketolysis biomarker genes ( Bdh1 , Oxct1 , Acaa2 ). B, Fatty acid oxidation biomarker genes. Results demonstrate relative preservation of metabolic gene expression in TKO infarct zones compared with WT infarct zones. While these metabolic genes were downregulated in infarct zones of both genotypes compared with non-infarct tissue, fold changes >1 indicate that TKO hearts maintained relatively higher expression levels, suggesting preserved metabolic capacity following myocardial infarction.

Article Snippet: These samples were submitted to Novogene for whole genome bisulfite sequencing, library preparation, and sequencing using their established protocols.

Techniques: RNA Sequencing, Gene Expression, Biomarker Discovery, Preserving, Expressing

Journal: bioRxiv

Article Title: TIGAR DEFICIENCY ENHANCES CARDIAC RESILIENCE THROUGH EPIGENETIC PROGRAMMING OF PARKIN EXPRESSION

doi: 10.1101/2025.07.14.664830

Figure Lengend Snippet: A, Integrative Genomics Viewer (IGV) visualization of the Prkn gene with whole-genome bisulfite sequencing (WGBS) and RNA-seq data from WT and TKO mice hearts under normal chow and HFD conditions, with corresponding RNA-seq analysis showing significantly increased Parkin (Prkn) mRNA expression in TKO-HFD vs WT-HFD hearts (B). C, Enlarged view of the differentially methylated region (DMR) within Prkn intron 10 (red dashed box, coordinates chr17:12,016,102-12,019,334, 3,233 bp). D, Quantification of methylated CpG sites in the DMR in Prkn intron 10 in WT (148±28) and TKO (58±24) heart tissues. *P=0.0139, n=3. E, CRISPR/Cas9-mediated deletion of a 14,177 bp fragment (chr17:12006677 to chr17:12020853) in Prkn intron 10 in C2C12 myoblasts (Mb) and 3T3-L1 fibroblasts (Fb). Agarose gel electrophoresis shows the predicted 1,185 bp PCR amplicon in P(i)10 -/- cells (gRNA/Cas9 vector transfected) vs the 2,422 bp band in scramble vector (Scr) transfected control cells. F-G, RT-qPCR analysis of Parkin mRNA levels in Prkn intron 10 DMR-deleted (P(i)10 -/-) and scramble control (Scr) C2C12 myoblasts (F) and 3T3-L1 fibroblasts (G), showing 10-fold and 5-fold increases, respectively, in Parkin expression following DMR deletion. Data represent mean±SD; **P<0.01; ***P<0.001; n=3 independent experiments.

Article Snippet: These samples were submitted to Novogene for whole genome bisulfite sequencing, library preparation, and sequencing using their established protocols.

Techniques: Methylation Sequencing, RNA Sequencing, Expressing, Methylation, CRISPR, Agarose Gel Electrophoresis, Amplification, Plasmid Preparation, Transfection, Control, Quantitative RT-PCR

Journal: bioRxiv

Article Title: TIGAR DEFICIENCY ENHANCES CARDIAC RESILIENCE THROUGH EPIGENETIC PROGRAMMING OF PARKIN EXPRESSION

doi: 10.1101/2025.07.14.664830

Figure Lengend Snippet: A-C, Echocardiograms and quantification of left ventricular ejection fraction (EF), mass (LVM), and end-diastolic volume (LVEDV) in 4-month-old male WT (n=10) and TKO mice (n=13) 4 weeks after myocardial infarction (MI). MI was induced by left anterior descending (LAD) artery ligation. Sham-operated mice served as controls. D-F, Echocardiograms and quantification of left ventricular ejection fraction (EF), mass (LVM), and end-diastolic volume (LVEDV) in 4-month-old male control Myh6Cre mice (n=6) and hTKO mice (n=4) 4 weeks after MI. G-H, RNA-seq analysis of mitochondrial-encoded genes (G) and nuclear-encoded mitochondrial genes (H) from the infarct zone, expressed as fold changes in TKO vs WT. I, Immunoblot analysis of TIGAR, Troponin I, SERCA2, α-actinin1, and Vinculin in infarcted heart tissue from WT and TKO mice, with normal left ventricular tissue (Control LV) as reference. J, RNA-seq analysis of cardiac marker genes from the infarct zone, expressed as fold changes in TKO vs WT. For RNA-seq analyses (G, H, J), RNA from 3 mice per group was pooled for sequencing. Data represent mean±SD; *P<0.05.

Article Snippet: In the first analysis, purified WT and TKO cardiac genomic DNA samples were submitted to Azenta Life Sciences for whole genome bisulfite sequencing.

Techniques: Ligation, Control, RNA Sequencing, Western Blot, Marker, Sequencing

Journal: bioRxiv

Article Title: TIGAR DEFICIENCY ENHANCES CARDIAC RESILIENCE THROUGH EPIGENETIC PROGRAMMING OF PARKIN EXPRESSION

doi: 10.1101/2025.07.14.664830

Figure Lengend Snippet: Representative immunofluorescence images of heart sections from WT and TKO mice showing sham myocardium, non-infarct myocardium, and infarct myocardium. Sections were stained for DAPI (blue, nuclei), α-actinin (green, cardiomyocytes), and periostin (red, fibrosis marker). B, RNA sequencing analysis of fibrosis marker genes Postn (periostin) and Lgals3 (galectin-3) in left ventricle (LV), infarct zone, border zone, and remote zone of WT and TKO hearts. TKO hearts demonstrated reduced expression of fibrosis markers in non-infarct (remote) myocardium compared with WT hearts.

Article Snippet: In the first analysis, purified WT and TKO cardiac genomic DNA samples were submitted to Azenta Life Sciences for whole genome bisulfite sequencing.

Techniques: Immunofluorescence, Staining, Marker, RNA Sequencing, Expressing

Journal: bioRxiv

Article Title: TIGAR DEFICIENCY ENHANCES CARDIAC RESILIENCE THROUGH EPIGENETIC PROGRAMMING OF PARKIN EXPRESSION

doi: 10.1101/2025.07.14.664830

Figure Lengend Snippet: RNA sequencing analysis comparing gene expression ratios (TKO-Infarct/WT-Infarct) in infarct zones. A, Ketolysis biomarker genes ( Bdh1 , Oxct1 , Acaa2 ). B, Fatty acid oxidation biomarker genes. Results demonstrate relative preservation of metabolic gene expression in TKO infarct zones compared with WT infarct zones. While these metabolic genes were downregulated in infarct zones of both genotypes compared with non-infarct tissue, fold changes >1 indicate that TKO hearts maintained relatively higher expression levels, suggesting preserved metabolic capacity following myocardial infarction.

Article Snippet: In the first analysis, purified WT and TKO cardiac genomic DNA samples were submitted to Azenta Life Sciences for whole genome bisulfite sequencing.

Techniques: RNA Sequencing, Gene Expression, Biomarker Discovery, Preserving, Expressing

Journal: bioRxiv

Article Title: TIGAR DEFICIENCY ENHANCES CARDIAC RESILIENCE THROUGH EPIGENETIC PROGRAMMING OF PARKIN EXPRESSION

doi: 10.1101/2025.07.14.664830

Figure Lengend Snippet: A, Integrative Genomics Viewer (IGV) visualization of the Prkn gene with whole-genome bisulfite sequencing (WGBS) and RNA-seq data from WT and TKO mice hearts under normal chow and HFD conditions, with corresponding RNA-seq analysis showing significantly increased Parkin (Prkn) mRNA expression in TKO-HFD vs WT-HFD hearts (B). C, Enlarged view of the differentially methylated region (DMR) within Prkn intron 10 (red dashed box, coordinates chr17:12,016,102-12,019,334, 3,233 bp). D, Quantification of methylated CpG sites in the DMR in Prkn intron 10 in WT (148±28) and TKO (58±24) heart tissues. *P=0.0139, n=3. E, CRISPR/Cas9-mediated deletion of a 14,177 bp fragment (chr17:12006677 to chr17:12020853) in Prkn intron 10 in C2C12 myoblasts (Mb) and 3T3-L1 fibroblasts (Fb). Agarose gel electrophoresis shows the predicted 1,185 bp PCR amplicon in P(i)10 -/- cells (gRNA/Cas9 vector transfected) vs the 2,422 bp band in scramble vector (Scr) transfected control cells. F-G, RT-qPCR analysis of Parkin mRNA levels in Prkn intron 10 DMR-deleted (P(i)10 -/-) and scramble control (Scr) C2C12 myoblasts (F) and 3T3-L1 fibroblasts (G), showing 10-fold and 5-fold increases, respectively, in Parkin expression following DMR deletion. Data represent mean±SD; **P<0.01; ***P<0.001; n=3 independent experiments.

Article Snippet: In the first analysis, purified WT and TKO cardiac genomic DNA samples were submitted to Azenta Life Sciences for whole genome bisulfite sequencing.

Techniques: Methylation Sequencing, RNA Sequencing, Expressing, Methylation, CRISPR, Agarose Gel Electrophoresis, Amplification, Plasmid Preparation, Transfection, Control, Quantitative RT-PCR