Sequence and parent-of-origin dependent m6A contribute to allele-specific gene expression [GLORI]
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ABSTRACT:
PROVIDER: PRJNA1105083 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28816546_1.fastq.gz | Fastqsanger.gz | |||
| SRR28816546_2.fastq.gz | Fastqsanger.gz | |||
| SRR28816547_1.fastq.gz | Fastqsanger.gz | |||
| SRR28816547_2.fastq.gz | Fastqsanger.gz |
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Project description:Multiple regulatory layers influence allele-specific expression (ASE), particularly through sequence-dependent and parent-of-origin-dependent mechanisms at the transcriptional level. However, little is known about allele-specific gene regulation at the post-transcriptional level. Here, we conduct transcriptome-wide analysis of allele-specific m6A in mice. Using early postnatal cerebellum and cerebrum samples from reciprocal crosses of two divergent mouse strains, we employed quantitative m6A assays to measure allelic differences in m6A at single-base resolution. Our study reveals widespread sequence-dependent allelic imbalance in m6A methylation, identifying thousands of allele-specific m6A (ASm6A) sites with statistically significant and reproducible allelic methylation differences across diverse samples. We find evidence of potential cis-regulatory variants within 50-nt flanking regions of these ASm6A sites, with the highest enrichment at the motif positions. Intriguingly, we detect parental effects on allelic methylation across m6A sites exhibiting parent-of-origin-dependent ASE. For both sequence- and parent-of-origin-dependent allelic m6A methylation, we observe opposing allelic preferences between methylation and expression, suggesting a potential role of ASm6A in regulating ASE through negative effects on gene expression. Overall, our findings reveal that both cis-acting and parent-of-origin effects influence ASm6A, offering new insights into post-transcriptional mechanisms of ASE regulation.
2024-04-26 | GSE265977 | GEO
Project description:Multiple regulatory layers influence allele-specific expression (ASE), particularly through sequence-dependent and parent-of-origin-dependent mechanisms at the transcriptional level. However, little is known about allele-specific gene regulation at the post-transcriptional level. Here, we conduct transcriptome-wide analysis of allele-specific m6A in mice. Using early postnatal cerebellum and cerebrum samples from reciprocal crosses of two divergent mouse strains, we employed quantitative m6A assays to measure allelic differences in m6A at single-base resolution. Our study reveals widespread sequence-dependent allelic imbalance in m6A methylation, identifying thousands of allele-specific m6A (ASm6A) sites with statistically significant and reproducible allelic methylation differences across diverse samples. We find evidence of potential cis-regulatory variants within 50-nt flanking regions of these ASm6A sites, with the highest enrichment at the motif positions. Intriguingly, we detect parental effects on allelic methylation across m6A sites exhibiting parent-of-origin-dependent ASE. For both sequence- and parent-of-origin-dependent allelic m6A methylation, we observe opposing allelic preferences between methylation and expression, suggesting a potential role of ASm6A in regulating ASE through negative effects on gene expression. Overall, our findings reveal that both cis-acting and parent-of-origin effects influence ASm6A, offering new insights into post-transcriptional mechanisms of ASE regulation.
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Project description:Sequence and parent-of-origin dependent m6A contribute to allele-specific gene expression [m6A-seq]
| PRJNA1105082 | ENA
Project description:Sequence and parent-of-origin dependent m6A contribute to allele-specific gene expression
| PRJNA1105078 | ENA
Project description:We looked for parent of origin effects on genome-wide gene expression in a reciprocal cross between C57BL/6J x B6(C)-H2bm12/KhEgJ mice (the latter strain is a knockout of H2-ab1 on a C57BL/6J background). The aim is to find genes whose expression is altered in trans depending on whether the mother or father carried a knockout allele for H2-ab1. In this experiment differential expression of a gene is inferred from a difference in its overall expression levels. We sequenced RNA from 30 F1 mice from the H2-ab1 heterozygous cross. Both heterozygous and wild type F1 animals were sequenced in order to find both parental and parent of origin effects. We measured expression in the lungs (average 6.2 million reads per sample) and hippocampus (6.6 million reads).
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Project description:This SuperSeries is composed of the SubSeries listed below.
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Project description:An allele of a gene can be epigenetically regulated to show a parent-of-origin biasedexpression pattern, a phenomenon referring to as genomic imprinting. Genomic imprinting ishighly tissue-specific, and mammalian brains are hotspots for this effect. Social behaviourdefects in human and various behavioural changes in mouse, had been linked toinappropriate imprinting, but little is known about how and why such effects occur.The olfactory system in the brain is the essential sensory circuitry that mediates rodent innatebehaviour. Meanwhile, monoallelic expression, a related process, is used extensively inchemosensory neurons to regulate olfactory and vomeronasal receptor choice. We have datashowing receptor gene choice is not a random process, which implies allele choice may bebiased also. The olfactory system is therefore a promising target for detecting allelicimbalance, or even novel imprinting genes, by high-resolution RNA-sequencing followed byallelic-specific transcriptomic mapping.This project is designed to detect parent-of-origin and strain-of-origin allelic expression bias inneurons from a key olfactory tissues in rodents: vomernasal organ (VNO) . RNA from reciprocally crossed F1 hybrid mice (S-cross and M-cross) from two distinct inbred strains (C57BL/6J and CAST) have been extracted respectively. After sequencing,expression levels from each allele will be distinguished by incorporating SNP and indeldifferences to the strain-specific reference genomes. Analysis will be carried out incollaboration with Gary Churchill's team at the Jackson Laboratory (who have developed amethod of analysing RNAseq data from CAST x C57BL/6J F1s).Genes with strong, reproducible allelic imbalances will be followed up to assess the functional consequences.
2014-12-09 | E-ERAD-318 | biostudies-arrayexpress
Project description:An allele of a gene can be epigenetically regulated to show a parent-of-origin biasedexpression pattern, a phenomenon referring to as genomic imprinting. Genomic imprinting ishighly tissue-specific, and mammalian brains are hotspots for this effect. Social behaviourdefects in human and various behavioural changes in mouse, had been linked toinappropriate imprinting, but little is known about how and why such effects occur.The olfactory system in the brain is the essential sensory circuitry that mediates rodent innatebehaviour. Meanwhile, monoallelic expression, a related process, is used extensively inchemosensory neurons to regulate olfactory and vomeronasal receptor choice. We have datashowing receptor gene choice is not a random process, which implies allele choice may bebiased also. The olfactory system is therefore a promising target for detecting allelicimbalance, or even novel imprinting genes, by high-resolution RNA-sequencing followed byallelic-specific transcriptomic mapping.This project is designed to detect parent-of-origin and strain-of-origin allelic expression bias inneurons from two olfactory tissues: main olfactory epithelium (MOE) and olfaction bulb (OB). RNA from reciprocally crossed F1 hybrid mice (S-cross and M-cross) from two distinct inbred strains (C57BL/6J and CAST) have been extracted respectively (two crosses, two tissue types). After sequencing,expression levels from each allele will be distinguished by incorporating SNP and indeldifferences to the strain-specific reference genomes. Analysis will be carried out incollaboration with Gary Churchill's team at the Jackson Laboratory (who have developed amethod of analysing RNAseq data from CAST x C57BL/6J F1s).Genes with strong, reproducible allelic imbalances will be followed up to assess the functional consequences.
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Project description:To investigate the epigenetic landscape at the interface between mother and fetus, we provide a comprehensive analysis of parent of origin bias in the placenta. Using F1 interspecies hybrids, we sequenced RNA from 23 individual midgestation placentas, five late stage placentas, and two yolk sac samples and then used SNPs to determine whether transcripts were preferentially generated from the maternal or paternal allele. In the placenta, we find 103 genes that show significant and reproducible parent-of-origin bias, of which 78 are novel candidates. Most (96%) show a strong maternal bias which, using multiple models, we demonstrate is not due to maternal decidual contamination. Analysis of the X chromosome also reveals paternal expression of Xist and several genes that escape inactivation, most significantly Rps4x, Fhl1, and Slc38a5. Finally, sequencing individual placentas allowed us to reveal notable expression similarity between littermates. In all, we observe a striking preference for maternal transcription in the midgestation mouse placenta and a dynamic imprinting landscape in extraembryonic tissues, reflecting the complex nature of epigenetic pathways in the placenta. 3'-end Sequencing for Expression Quantification (3SEQ) and SNP Analysis to observe parent-of-origin bias in 28 placental samples at two time points and 2 yolk sac samples
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