Characterization of imprinted genes in rice reveals regulation and imprinting conservation at some loci in plant species
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ABSTRACT:
PROVIDER: PRJNA453967 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7073540_1.fastq.gz | Fastqsanger.gz | |||
| SRR7073540_2.fastq.gz | Fastqsanger.gz | |||
| SRR7073541_1.fastq.gz | Fastqsanger.gz | |||
| SRR7073541_2.fastq.gz | Fastqsanger.gz | |||
| SRR7073542_1.fastq.gz | Fastqsanger.gz |
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Project description:Genomic imprinting is an epigenetic phenomenon by which certain genes display differential expression in a parent-of-origin-dependent manner. Hundreds of imprinted genes have been identified from several plant species. Here we identified, with a high level of confidence, 208 imprinted candidates from rice. Imprinted genes of rice showed limited association to the transposable elements, which contrasts with findings from Arabidopsis. Generally, imprinting in rice is conserved within species, but intraspecific variation was detected as well.
2018-05-15 | GSE113769 | GEO
Project description:Mouse embryo fibroblasts (MEFs) closely resemble mouse embryos and are convenient sources for biochemical studies when cell number may be limiting from mouse embryos. To derive the imprinting signature of MEFs and potentially detect novel imprinted genes we characterized them using strand- and allele-specific RNA deep sequencing. We used Sequenom allelotyping in embryo and adult organs to verify parental allele-specific expression patterns. We found correct parental allele-specific transcription of 32 known ubiquitously imprinted genes in MEFs. Our analysis did not reveal any novel imprinted genes in MEFs, but detected extended parental allele-specific transcription in several known imprinted domains: maternal allele-specific transcription downstream of Grb10 and downstream of Meg3, Rtl1as and Rian in the Dlk1-Dio3 cluster, an imprinted domain implicated in development. We detected paternal allele-specific transcription downstream of Nespas, Peg3, Peg12 and Snurf/Snrpn. These imprinted transcript extensions were not unique to MEFs, but were also present in other somatic cells. Their 5’ end points did not carry opposing chromatin marks or parental allele-specific DNA methylation, suggesting that their parental allele-specific transcription is under the control of the extended genes. Based on the imprinting signature of MEFs, they provide valid models for understanding the biochemical aspects of genomic imprinting. Strand-specific and parental allele-specific RNA-seq was done in female mouse embryo fibroblasts.
2013-11-18 | E-GEOD-49538 | biostudies-arrayexpress
Project description:It is increasingly being recognized that physical interactions between distant chromosomal loci influence the expressivity of the genome. Thus, multiple enhancers may converge on a single gene promoter 1,2 and a single enhancer can stochastically loop to multiple promoters 3. Regulatory elements from neighboring domains or from other chromosomes may interact to generate chromatin structures poised for transcription4-8 or repression 9-11. However, a broader perspective on the formation and function of such networks remains largely unexplored. Using the high-resolution 4C (Circular Chromosome Conformation Capture) analysis, we identify here a genome-wide physical network between genomically imprinted domains impinging H19 imprinting control region (ICR). Sequences interacting with the H19 ICR constitutively map at or within most of known imprinted domains both in mouse embryonic stem cells and in vitro-derived embryoid bodies, despite distinct differences in chromatin environments. Moreover, all-to-all 3D DNA FISH analyses revealed that imprinted domains from 7 different chromosomes co-localize with each other in pair-wise patterns, highlighting the dynamic nature of these interactions. The observed interaction network is dependent on CTCF binding sites within the maternally inherited H19 ICR allele and delays reprogramming of epigenetic features at imprinted domains during male germline development. As other imprinted regions can interact with each other in an H19 ICR-dependent manner, the H19 ICR emerges as an organizer of chromosomal networks by specifically recognizing and reconfiguring imprinted domains. We propose that an ancient key regulatory region, such as the H19 ICR, gradually impacted epigenetic modifications via long-range interactions in the germline to facilitate the recruitment of imprinted genes and their formation in clusters during mammalian radiation. Furthermore, the perspective of epigenetic lesions de-stabilizing such chromosomal networks may advance our understanding of how quantitative traits influence human diseases, such as cancer.
2009-12-14 | GSE14074 | GEO
Project description:Mouse embryo fibroblasts (MEFs) closely resemble mouse embryos and are convenient sources for biochemical studies when cell number may be limiting from mouse embryos. To derive the imprinting signature of MEFs and potentially detect novel imprinted genes we characterized them using strand- and allele-specific RNA deep sequencing. We used Sequenom allelotyping in embryo and adult organs to verify parental allele-specific expression patterns. We found correct parental allele-specific transcription of 32 known ubiquitously imprinted genes in MEFs. Our analysis did not reveal any novel imprinted genes in MEFs, but detected extended parental allele-specific transcription in several known imprinted domains: maternal allele-specific transcription downstream of Grb10 and downstream of Meg3, Rtl1as and Rian in the Dlk1-Dio3 cluster, an imprinted domain implicated in development. We detected paternal allele-specific transcription downstream of Nespas, Peg3, Peg12 and Snurf/Snrpn. These imprinted transcript extensions were not unique to MEFs, but were also present in other somatic cells. Their 5’ end points did not carry opposing chromatin marks or parental allele-specific DNA methylation, suggesting that their parental allele-specific transcription is under the control of the extended genes. Based on the imprinting signature of MEFs, they provide valid models for understanding the biochemical aspects of genomic imprinting.
2013-11-18 | GSE49538 | GEO
Project description:Genomic imprinting is the parent-of-origin-specific allelic transcriptional silencing observed in mammals, which is governed by DNA methylation established in the gametes and maintained throughout the development. The frequency and extent of epimutations associated with the nine reported imprinting syndromes varies because it is evident that aberrant preimplantation maintenance of imprinted differentially methylated regions (DMRs) may affect multiple loci. Using a custom Illumina GoldenGate array targeting 27 imprinted DMRs, we profiled allelic methylation in 8 imprinting defect patients.
2022-07-01 | GSE198925 | GEO
Project description:Genomic imprinting is a mechanism in which the expression of genes varies depending on their parent-of-origin. Imprinting occurs through differential DNA methylation and histone modifications on the two parental alleles, with most imprinted genes marked by CpG-rich differentially methylated regions (DMRs). DNA methylation profiling in cases of uniparental disomy (UPD) provides a unique system permitting the study of DNA derived from a single parent (PMID: 20631049). Approximately 70 human imprinted genes have been described, and imprinted loci have been associated with diseases such as diabetes and cancer. We profiled parent of origin DNA methylation marks to find novel imprinted loci. Methods: We have an unprecedented collection of whole blood DNA from XX patients with UPD covering 18 different chromosomes, allowing for the efficient detection of DMRs associated with imprinted genes for 84% of the human genome. Our study is complimented with Ovarian Teratoma DNA (maternal DNA) and Complete hydatidiform Mole (paternal DNA). DNA methylation was profiled using Illumina Infinium 450K Methylation BeadArrays. Imprinted DMRs were defined by sites at which the maternal and paternal methylation levels diverged significantly from the biparental average. We confirmed novel DMRs by bisulfite sequencing of informative trios and SequenomEpiTYPER assays. Allelic specific gene expression studies were also performed by RNA sequencing in independent biparental controls. Findings: Our results provide for the first comprehensive map of the human imprintome, doubling the number of known imprinted regions. We identified a total of 71 DMRs, 41 of which were novel. 27 novel DMRs were maternally methylated and 14 were paternally methylated. We identified DMRs on chromosomes 5, 21 and 22 previously considered devoid of imprinting, highlighting potential parent-of-origin effects in chromosomal aneuploidies such as Down syndrome. We also found DMRs in genes associated with Schizophrenia and epilepsy. Interpretation: Our data provide the first comprehensive genome-wide map of imprinted sites in the human genome, and provide novel insights into potential parent-of-origin effects in human disorders. 66 UPD samples analyzed in total, From each individual, whole bllod DNA was extracted and global DNA methylation levels were assessed using Illumina Infinium HumanMethylation450 BeadChip.
2016-06-01 | E-GEOD-64244 | biostudies-arrayexpress
Project description:Genomic imprinting is a critical developmental process characteristic of parent-of-origin- specific gene expression. Here, we have identified the AFF family protein, Aff3, as a factor that functionally interacts with imprinted loci. Indeed, our genome-wide studies demonstrate that Aff3 specifically binds both imprinting control regions (ICRs) and enhancers within imprinted loci in an allele-specific manner. We have identified the molecular regulators involved in the recruitment of Aff3 to ICRs to impede transcription through the ICR, and provide a mechanism requiring Aff3 within the Super Elongation Complex-like 3 (SEC-L3) in the expression of an imprinted polycistronic transcript spanning the Dlk1-Dio3 locus. Our study also shows that DNA methylation at the ICR reinforces silencing of its related enhancers by controlling the binding and activity of Aff3 in an allele-specific manner. This study provides molecular details about the regulation of dosage-critical imprinted gene expression through Aff3’s function in transcriptional elongation control.
2016-01-01 | GSE64489 | GEO
Project description:To understand the evolution of imprinting mechanisms in the rice species Oryza sativa, we analyzed DNA methylation, transcription and small RNA expression in embryo and endosperm. Cultivars chosen to represent the genetic diversity of cultivated Oryza sativa comprised Nipponbare and Kitaake of the japonica subspecies, and IR64 and 93-11 cultivars of the indica subspecies. While imprinted expression is generally conserved among rice cultivars, approximately 10% of imprinted genes show imprinting divergence across the four cultivars. Analyses of DNA methylation and small RNAs revealed that small RNA producing loci are closely associated with genic regions and four times more likely to be imprinted than genes. However, imprinting divergence most often correlated with DNA methylation epimutations. Correlative epialleles were largely stable within subspecies. Small indels and transposable element insertions were found at half of the epimutated loci and associated with imprinting divergence at half of the remaining loci. Correlating epigenetic and genetic variation occurred at key regulatory regions – the promoter and transcription start site of maternally-biased genes, and the promoter and gene body of paternally-biased genes. Our results reinforce models for the role of maternal-specific DNA hypomethylation in imprint formation at both maternally and paternally biased genes, and highlight the role of transposition events and epimutation in rice imprinting evolution.
2021-06-29 | GSE130122 | GEO
Project description:In plants, imprinted gene expression occurs in endosperm seed tissue and can be associated with differential DNA methylation between maternal and paternal alleles. Imprinting is theorized to have been selected for because of conflict between parental genomes in offspring, but most studies of imprinting have been conducted in Arabidopsis thaliana, an inbred primarily self-fertilizing species that should have limited parental conflict. We examined embryo and endosperm allele-specific expression and DNA methylation genome-wide in the wild outcrossing species Arabidopsis lyrata. Here we show that the majority of A. lyrata imprinted genes exhibit parentally-biased expression in A. thaliana, suggesting that there is evolutionary conservation in gene imprinting. Surprisingly, we discovered substantial interspecies differences in methylation features associated with paternally expressed imprinted genes (PEGs). Unlike A. thaliana, the maternal allele of many A. lyrata PEGs was hypermethylated in the CHG context. Increased maternal allele CHG methylation was associated with increased expression bias in favor of the paternal allele. We propose that CHG methylation maintains or reinforces repression of maternal alleles of PEGs. These data suggest that while the genes subject to imprinting are largely conserved, there is flexibility in the epigenetic mechanisms employed between closely related species to maintain monoallelic expression. This supports the idea that imprinting of specific genes is a functional phenomenon, and not simply a byproduct of seed epigenomic reprogramming.
2016-09-01 | GSE76076 | GEO
Project description:Genomic imprinting is a critical developmental process characteristic of parent-of-origin- specific gene expression. Here, we have identified the AFF family protein, Aff3, as a factor that functionally interacts with imprinted loci. Indeed, our genome-wide studies demonstrate that Aff3 specifically binds both imprinting control regions (ICRs) and enhancers within imprinted loci in an allele-specific manner. We have identified the molecular regulators involved in the recruitment of Aff3 to ICRs to impede transcription through the ICR, and provide a mechanism requiring Aff3 within the Super Elongation Complex-like 3 (SEC-L3) in the expression of an imprinted polycistronic transcript spanning the Dlk1-Dio3 locus. Our study also shows that DNA methylation at the ICR reinforces silencing of its related enhancers by controlling the binding and activity of Aff3 in an allele-specific manner. This study provides molecular details about the regulation of dosage-critical imprinted gene expression through Aff3âs function in transcriptional elongation control. ChIP-seq of Aff3 in different mES cells. ChIP-seq of Aff3, PolII, H3K9me3 in uniparental MEF cell lines. ChIP-seq of H3K27ac and PolII in mES cells after Aff3 shRNA and non-targeting shRNA. ChIP-seq of H3K27ac in wild type and Zfp57 knockout ES cells. Total RNA-seq and nascent RNA-seq of mES cells after Aff3 shRNA and non-targeting shRNA. Total RNA-seq of uniparental MEF cells after Aff3 shRNA and non-targeting shRNA.
2016-07-03 | E-GEOD-64489 | biostudies-arrayexpress