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Series GSE244207 Query DataSets for GSE244207
Status Public on Mar 14, 2024
Title ATAC and histone H3K9me3 landscapes reveal long-term epigenomic effects of fetal-neonatal iron deficiency in rat hippocampus [ChIP-seq]
Organism Rattus norvegicus
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary Background: Iron deficiency (ID) during the fetal-neonatal period results in long-term neurodevelopmental impairments associated with pervasive hippocampal gene dysregulation. Prenatal choline supplementation partially normalizes these effects, suggesting an interaction between iron and choline in hippocampal transcriptome regulation. To understand the regulatory mechanisms, we investigated epigenetic marks of genes that are poised to be activated (ATAC-seq) or repressed (H3K9me3 ChIP-seq) in iron-repleted adult rats having experienced fetal-neonatal ID exposure with or without prenatal choline supplementation. Results: Fetal-neonatal ID was induced by limiting maternal iron intake from gestational day (G) 2 through postnatal day (P) 7. Half of the pregnant dams were given supplemental choline (5.0 g/kg) from G11-18. This resulted in 4 groups at P65 (Iron-sufficient [IS], Formerly Iron-deficient [FID], IS with choline [ISch], and FID with choline [FIDch]). Hippocampi were collected from P65 iron-repleted male offspring and analyzed for chromatin accessibility and H3K9me3 enrichment. 22% and 24% of differentially transcribed genes in FID- and FIDch-groups, respectively, exhibited significant differences in chromatin accessibility, whereas 1.7% and 13% exhibited significant differences in H3K9me3 enrichment. These changes mapped onto gene networks regulating synaptic plasticity, neuroinflammation, and reward circuits. Motif analysis of differentially modified genomic sites revealed significantly stronger choline effects than early-life ID and identified multiple epigenetically modified transcription factor binding sites. Conclusions: This study reveals genome-wide, stable epigenetic changes and epigenetically modifiable gene networks associated with specific chromatin marks in the hippocampus, and lays a foundation to further elucidate iron-dependent epigenetic mechanisms that underlie the long-term effects of fetal-neonatal ID, choline, and their interactions.
 
Overall design To generate 4 dietary groups, pregnant and nursing rats were fed iron-sufficient or iron-deficient diet from gestational day (G) 2 to postnatal day (P) 7 with or without supplemental choline from G11-18. Hippocampi from P65 male offspring were analyzed.
 
Contributor(s) Liu SX, Ramakrishnan A, Shen L, Gewirtz JC, Georgieff MK, Tran PV
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Submission date Sep 27, 2023
Last update date Mar 14, 2024
Contact name Aarthi Ramakrishnan
E-mail(s) [email protected]
Organization name Icahn School of Medicine at Mount Sinai
Department Neuroscience
Street address 1425 Madison Avenue
City New York
State/province New York
ZIP/Postal code 10029
Country USA
 
Platforms (1)
GPL18694 Illumina HiSeq 2500 (Rattus norvegicus)
Samples (16)
GSM7808602 Hippocampus, K9me3-P65ID10_S9
GSM7808603 Hippocampus, K9me3-P65ID11B_S10
GSM7808604 Hippocampus, K9me3-P65ID-pooled1_S4
This SubSeries is part of SuperSeries:
GSE244208 ATAC and histone H3K9me3 landscapes reveal long-term epigenomic effects of fetal-neonatal iron deficiency in rat hippocampus
Relations
BioProject PRJNA1021662

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Supplementary file Size Download File type/resource
GSE244207_annotated_IDC_peaks_chipseq.txt.gz 70.5 Kb (ftp)(http) TXT
GSE244207_annotated_ID_peaks_chipseq.txt.gz 261.6 Kb (ftp)(http) TXT
GSE244207_annotated_ISC_peaks_chipseq.txt.gz 66.3 Kb (ftp)(http) TXT
GSE244207_annotated_IS_peaks_chipseq.txt.gz 628.0 Kb (ftp)(http) TXT
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