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44 results for “monoallelic”
Data from: Chromatin signature of widespread monoallelic expression
In mammals, numerous autosomal genes are subject to mitotically stable monoallelic expression (MAE), including genes that play critical roles in a variety of human diseases. Due to challenges posed by the clonal nature of MAE, very little is known about its regulation; in particular, no molecular features have been specifically linked to MAE. Here we report an approach that distinguishes MAE genes in human cells with great accuracy: a chromatin signature consisting of chromatin marks associated with active transcription (H3K36me3) and silencing (H3K27me3) simultaneously occurring in the gene body. The MAE signature is present in ~20% of ubiquitously expressed genes and over 30% of tissue-specific genes across cell types. Notably, it is enriched among key developmental genes that have bivalent chromatin structure in pluripotent cells. Our results open a new approach to the study of MAE that is independent of polymorphisms, and suggest that MAE is linked to cell differentiation.
Data from: Chromatin signature of widespread monoallelic expression
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Data from: Monoallelic loss of the imprinted gene Grb10 promotes tumor formation in irradiated Nf1+/- mice
Imprinted genes are expressed from only one parental allele and heterozygous loss involving the expressed allele is sufficient to produce complete loss of protein expression. Genetic alterations are common in tumorigenesis but the role of imprinted genes in this process is not well understood. In earlier work we mutagenized mice heterozygous for the Neurofibromatosis I tumor suppressor gene (NF1) to model radiotherapy-associated second malignant neoplasms that arise in irradiated NF1 patients. Expression analysis of tumor cell lines established from our mouse models identified Grb10 expression as widely absent. Grb10 is an imprinted gene and polymorphism analysis of cell lines and primary tumors demonstrates that the expressed allele is commonly lost in diverse Nf1 mutant tumors arising in our mouse models. We performed functional studies to test whether Grb10 restoration or loss alter fundamental features of the tumor growth. Restoring Grb10 in Nf1 mutant tumors decreases proliferation, decreases soft agar colony formation and downregulates Ras signaling. Conversely, Grb10 silencing in untransformed mouse embryo fibroblasts significantly increased cell proliferation and increased Ras-GTP levels. Expression of a constitutively activated MEK rescued tumor cells from Grb10-mediated reduction in colony formation. These studies reveal that Grb10 loss can occur during in vivo tumorigenesis, with a functional consequence in untransformed primary cells. In tumors, Grb10 loss independently promotes Ras pathway hyperactivation, which promotes hyperproliferation, an early feature of tumor development. In the context of a robust Nf1 mutant mouse model of cancer this work identifies a novel role for an imprinted gene in tumorigenesis.
Data from: Monoallelic loss of the imprinted gene Grb10 promotes tumor formation in irradiated Nf1+/- mice
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Comparative analysis of gene expression of SLC3A2 monoallelic knockout and wild type clones
GEO Series GSE116162. Homo sapiens. 12 samples. Type: Expression profiling by array.
The developmental dynamics and disease potential of random monoallelic gene expression
GEO Series GSE54016. Mus musculus. 12 samples. Type: Expression profiling by high throughput sequencing.
Sex-biased and random monoallelic expression of SHOX: implications for sex difference in height
GEO Series GSE188531. Homo sapiens. 25 samples. Type: Expression profiling by array; Methylation profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other.
Landscape of Monoallelic DNA Accessibility and Gene Regulatory Networks during Reprogramming to Naive Pluripotency and X Chromosome Reactivation [ATAC-seq]
GEO Series GSE153844. Mus musculus. 6 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Impact of USP28 monoallelic deletion in HG3 CLL-derived cells
GEO Series GSE229756. Homo sapiens. 4 samples. Type: Expression profiling by high throughput sequencing.
Landscape of Monoallelic DNA Accessibility and Gene Regulatory Networks during Reprogramming to Naive Pluripotency and X Chromosome Reactivation [smart-seq]
GEO Series GSE153846. Mus musculus. 672 samples. Type: Expression profiling by high throughput sequencing.
Allele-specific differential regulation of monoallelically expressed autosomal genes in the cardiac lineage (scRNA-Seq)
GEO Series GSE173402. Mus musculus. 3 samples. Type: Expression profiling by high throughput sequencing.
Chromatin signature identifies monoallelic gene expression across mammalian cell types
GEO Series GSE67384. Mus musculus. 7 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
Genetic and Epigenetic Regulation of Pvt1 Monoallelic Expression [Hi-ChIP-seq]
GEO Series GSE287457. Mus musculus. 1 samples. Type: Other.
Genetic and Epigenetic Regulation of Pvt1 Monoallelic Expression
GEO Series GSE287458. Mus musculus. 101 samples. Type: Expression profiling by high throughput sequencing.
Chromatin signature identifies monoallelic gene expression across mammalian cell types (RNA-seq)
GEO Series GSE67379. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
Landscape of Monoallelic DNA Accessibility and Gene Regulatory Networks during Reprogramming to Naive Pluripotency and X Chromosome Reactivation [allele-specific analysis]
GEO Series GSE184987. Mus musculus. 47 samples. Type: Expression profiling by high throughput sequencing.
Using RNA sequencing for identifying gene imprinting and random monoallelic expression in human placenta (SNP genotyping)
GEO Series GSE56685. Homo sapiens. 30 samples. Type: SNP genotyping by SNP array; Genome variation profiling by SNP array.
Allele-specific differential regulation of monoallelically expressed autosomal genes in the cardiac lineage
GEO Series GSE173403. Mus musculus. 16 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
Allele-specific differential regulation of monoallelically expressed autosomal genes in the cardiac lineage (Bulk RNA-Seq)
GEO Series GSE173400. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Data from: Monoallelic chromatin conformation flanking long-range silenced domains in cancer-derived and normal cells
Epigenetic inactivation of chromatin plays an important role in determining cell phenotype in both normal and cancer cells, but our knowledge is still incomplete with respect to any potential monoallelic nature of the phenomenon. We have genotyped DNA isolated from chromatin of two colorectal cancer-derived lines and a culture of normal human intestinal epithelial cells (HIEC), which was immunoprecipitated with antibodies to acetylated vs. methylated histone H3K9, and presented the data as B allele frequency differences over multiple single-nucleotide polymorphism (SNP) moving window averages. [B allele is an arbitrary term defined as one of the two alleles at any given SNP, named A and B]. Three different validation tests confirmed that peaks exhibiting differences represented monoallelic domains. These complementary tests confirmed the following: 1) genes in the regions of high B allele frequency difference were expressed monoallelically; 2) in normal cells all five imprinting control regions which carried heterozygous SNPs were characterized by B allele difference peaks; and 3) the haplotypes in the B allele difference peaks were faithfully maintained in the chromatin immunoprecipitated with the respective antibodies. In both samples most of the monoallelic domains were found at the boundaries between regions of open and closed chromatin. With respect to the cancer line, this supports the established concept of conformation spreading, but the results from the normal cells were unexpected. Since these cells were polyclonal, the monoallelic structures were probably not determined by random choice as occurs in X-inactivation, so we propose that epigenetic inactivation in some domains may be heritable and polymorphic in normal human cells.
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Allen Brain Atlas
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DANDI Archive for NWB datasets
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.