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  • 1
    Online Resource
    Online Resource
    Chromatin Signature Identifies Monoallelic Gene Expression Across Mammalian Cell Types
    Oxford University Press (OUP) ; 2015
    In:  G3 Genes|Genomes|Genetics Vol. 5, No. 8 ( 2015-08-01), p. 1713-1720
    Details
    In: G3 Genes|Genomes|Genetics, Oxford University Press (OUP), Vol. 5, No. 8 ( 2015-08-01), p. 1713-1720
    Abstract: Monoallelic expression of autosomal genes (MAE) is a widespread epigenetic phenomenon which is poorly understood, due in part to current limitations of genome-wide approaches for assessing it. Recently, we reported that a specific histone modification signature is strongly associated with MAE and demonstrated that it can serve as a proxy of MAE in human lymphoblastoid cells. Here, we use murine cells to establish that this chromatin signature is conserved between mouse and human and is associated with MAE in multiple cell types. Our analyses reveal extensive conservation in the identity of MAE genes between the two species. By analyzing MAE chromatin signature in a large number of cell and tissue types, we show that it remains consistent during terminal cell differentiation and is predominant among cell-type specific genes, suggesting a link between MAE and specification of cell identity.
    Type of Medium: Online Resource
    ISSN: 2160-1836
    URL: Article
    DOI: 10.1534/g3.115.018853
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2015
    detail.hit.zdb_id: 2629978-1
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  • 2
    Online Resource
    Online Resource
    dbMAE: the database of autosomal monoallelic expression
    Oxford University Press (OUP) ; 2016
    In:  Nucleic Acids Research Vol. 44, No. D1 ( 2016-01-04), p. D753-D756
    Details
    In: Nucleic Acids Research, Oxford University Press (OUP), Vol. 44, No. D1 ( 2016-01-04), p. D753-D756
    Abstract: Recently, data on ‘random’ autosomal monoallelic expression has become available for the entire genome in multiple human and mouse tissues and cell types, creating a need for better access and dissemination. The database of autosomal monoallelic expression (dbMAE; https://mae.hms.harvard.edu) incorporates data from multiple recent reports of genome-wide analyses. These include transcriptome-wide analyses of allelic imbalance in clonal cell populations based on sequence polymorphisms, as well as indirect identification, based on a specific chromatin signature present in MAE gene bodies. Currently, dbMAE contains transcriptome-wide chromatin identification calls for 8 human and 21 mouse tissues, and describes over 16 000 murine and ∼700 human cases of directly measured biased expression, compiled from allele-specific RNA-seq and genotyping array data. All data are manually curated. To ensure cross-publication uniformity, we performed re-analysis of transcriptome-wide RNA-seq data using the same pipeline. Data are accessed through an interface that allows for basic and advanced searches; all source references, including raw data, are clearly described and hyperlinked. This ensures the utility of the resource as an initial screening tool for those interested in investigating the role of monoallelic expression in their specific genes and tissues of interest.
    Type of Medium: Online Resource
    ISSN: 1362-4962 , 0305-1048
    URL: Article
    DOI: 10.1093/nar/gkv1106
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2016
    detail.hit.zdb_id: 1472175-2
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Foreign RNA spike-ins enable accurate allele-specific expression analysis at scale
    Oxford University Press (OUP) ; 2023
    In:  Bioinformatics Vol. 39, No. Supplement_1 ( 2023-06-30), p. i431-i439
    Details
    In: Bioinformatics, Oxford University Press (OUP), Vol. 39, No. Supplement_1 ( 2023-06-30), p. i431-i439
    Abstract: Analysis of allele-specific expression is strongly affected by the technical noise present in RNA-seq experiments. Previously, we showed that technical replicates can be used for precise estimates of this noise, and we provided a tool for correction of technical noise in allele-specific expression analysis. This approach is very accurate but costly due to the need for two or more replicates of each library. Here, we develop a spike-in approach which is highly accurate at only a small fraction of the cost. Results We show that a distinct RNA added as a spike-in before library preparation reflects technical noise of the whole library and can be used in large batches of samples. We experimentally demonstrate the effectiveness of this approach using combinations of RNA from species distinguishable by alignment, namely, mouse, human, and Caenorhabditis elegans. Our new approach, controlFreq, enables highly accurate and computationally efficient analysis of allele-specific expression in (and between) arbitrarily large studies at an overall cost increase of ∼5%. Availability and implementation Analysis pipeline for this approach is available at GitHub as R package controlFreq (github.com/gimelbrantlab/controlFreq).
    Type of Medium: Online Resource
    ISSN: 1367-4803 , 1367-4811
    URL: Article
    DOI: 10.1093/bioinformatics/btad254
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1468345-3
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    CLONAL EPIGENETIC MOSAICISM: MECHANISM FOR CROHN’S DISEASE HETEROGENEITY
    Oxford University Press (OUP) ; 2021
    In:  Inflammatory Bowel Diseases Vol. 27, No. Supplement_1 ( 2021-01-21), p. S28-S28
    Details
    In: Inflammatory Bowel Diseases, Oxford University Press (OUP), Vol. 27, No. Supplement_1 ( 2021-01-21), p. S28-S28
    Abstract: Crohn’s disease is a chronic heterogenous disorder with patients showing complex phenotypes and highly variable response to therapies. GWAS studies have identified hundreds of genetic factors associated with the disease but the precise mechanism with which these genes cause variable phenotype in the disease are unknown. We observed an autosomal analog of X-chromosome inactivation causes clonally stable epigenetic mosaicism in intestinal organoids generated from mice. This epigenetic mosaicism was detected by measuring allele specific expression in organoids grown from different individuals and from spatially different regions of the mouse intestine. This epigenetic mechanism has been observed in more than 25% of autosomal genes in mouse and in human cell lines and is called autosomal monoallelic expression (MAE). Allelic imbalance in MAE genes is clonally stable, persisting for multiple organoid passages and is regulated partially by DNA methylation. Our findings suggest how non-genetic variation leads to formation of developmental clones (or patches) within an individual that could then cause a wide range of functional diversity, thereby driving phenotypic variability. This will point the ways to affect epigenetic differences in intestinal tissue for disease prevention.
    Type of Medium: Online Resource
    ISSN: 1078-0998 , 1536-4844
    URL: Article
    DOI: 10.1093/ibd/izaa347.066
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
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  • 5
    Online Resource
    Online Resource
    RNA sequencing-based screen for reactivation of silenced alleles of autosomal genes
    Oxford University Press (OUP) ; 2022
    In:  G3 Genes|Genomes|Genetics Vol. 12, No. 2 ( 2022-02-04)
    Details
    In: G3 Genes|Genomes|Genetics, Oxford University Press (OUP), Vol. 12, No. 2 ( 2022-02-04)
    Abstract: In mammalian cells, maternal and paternal alleles usually have similar transcriptional activity. Epigenetic mechanisms such as X-chromosome inactivation (XCI) and imprinting were historically viewed as rare exceptions to this rule. Discovery of autosomal monoallelic autosomal expression (MAE) a decade ago revealed an additional allele-specific mode regulating thousands of mammalian genes. Despite MAE prevalence, its mechanistic basis remains unknown. Using an RNA sequencing-based screen for reactivation of silenced alleles, we identified DNA methylation as key mechanism of MAE mitotic maintenance. In contrast with the all-or-nothing allelic choice in XCI, allele-specific expression in MAE loci is tunable, with exact allelic imbalance dependent on the extent of DNA methylation. In a subset of MAE genes, allelic imbalance was insensitive to DNA demethylation, implicating additional mechanisms in MAE maintenance in these loci. Our findings identify a key mechanism of MAE maintenance and provide basis for understanding the biological role of MAE.
    Type of Medium: Online Resource
    ISSN: 2160-1836
    URL: Article
    DOI: 10.1093/g3journal/jkab428
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2629978-1
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