Lamina Associated Domains in MEFs depleted of specific lamin isotypes
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ABSTRACT:
PROVIDER: PRJNA644536 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12162920.fastq.gz | Fastqsanger.gz | |||
| SRR12162921.fastq.gz | Fastqsanger.gz | |||
| SRR12162922.fastq.gz | Fastqsanger.gz | |||
| SRR12162923.fastq.gz | Fastqsanger.gz | |||
| SRR12162924.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: To compare the effects on Lamina Associated Domains (LADs) of shRNA treatment against lamin isotypes. Results: Using an optimized data analysis workflow (LADetector, available at https://github.com/thereddylab/LADetector), We found near identical sequences within the genome-wide maps indicating that ensemble methods are not effective for measuring random perturbations - perturbations that vary from cell to cell.
2020-07-07 | GSE153919 | GEO
Project description:The nuclear lamina is a proteinaceous network of filaments that provide both structural and gene regulatory functions by tethering proteins and large domains of DNA, so-called lamin associated domains (LADs), to the periphery of the nucleus. LADs are a large fraction of the mammalian genome that are repressed, in part, by their association to the nuclear periphery. The genesis and maintenance of LADs is poorly understood as are the proteins that participate in these functions. In an effort to identify proteins that reside at the nuclear periphery and potentially interact with LADs, we have taken a two-pronged approach. First, we have undertaken an interactome analysis of the inner nuclear membrane bound LAP2β to further characterize the nuclear lamina proteome. To accomplish this, we have leveraged the BioID system, which previously has been successfully used to characterize the nuclear lamina proteome. Second, we have established a system to identify proteins that bind to LADs by developing a chromatin directed BioID system. We combined the BioID system with the m6A-tracer system which binds to LADs in live cells to identify LAD proximal and nuclear lamina proteins. In combining these datasets, we have further characterized the protein network at the nuclear lamina as well as identified putative LAD proximal proteins. Our analysis identifies many heterochromatin related proteins related to H3K9 methylation processes as well as many proteins related to cell cycle regulation identifying important proteins essential for LAD function.
2021-03-09 | PXD012943 | Pride
Project description:Purpose: Many mammalian genes exhibit circadian expression patterns concordant with periodic binding of transcription factors, chromatin modifications and chromosomal interactions. We determined whether lamina-associated domains (LADs) display oscillatory circadian patterns of interaction with nuclear lamin B1 during hte circadian cycle, and identified any relationship to changes in gene expression patterns in oscillatory LADs or in their vinicity. Methods: To this end, we mapped LADs by chromatin immunoprecipitation-sequencing (ChIP-seq) of lamin B1 (LMNB1) (antibody ab16048, Abcam) from mouse livers colected every 6 h, for 30 h, after entrainment of the circadian clock by 24-h fasting and refeeding. Gene expression profiles were also analyzed by RNA-sequencing (RNA-seq) at the same time points. Results and Conclusions: We report periodic interactions of chromatin domains with nuclear lamin B1, suggesting rhythmic associations of fractions of the genome with the nuclear lamina. Entrainment of the circadian clock by fasting and refeeding is accompanied in mouse liver by a gain of lamin-chromatin interactions followed by oscillations in these interactions at hundreds of lamina-associated domains (LADs). A subset of these oscillations exhibit periodicity and affect one or both LAD borders or entire stand-alone LADs. Periodic LADs are however not a dominant feature of these variable LADs, as most LADs are conserved during the circadian cycle. LAD oscillations are for the most part asynchronous between the 5’ and 3’ ends of LADs. Periodic LADs also uncoupled from gene expression patterns, periodic or not, within or in vicinity of these LADs. Accordingly, periodic genes, including central clock-control genes, are located megabases away from LADs, suggesting their residence in a transcriptionally permissive environment throughout the circadian cycle. Our data suggest autonomous oscillatory associations of fractions of the genome with the nuclear lamina, providing new evidence for rhythmic spatial configurations of chromatin. However, our data also argue that periodic LADs constitute a minor fraction of variable LADs, and reflect stochasticity in variable lamin-chromatin interactions during the circadian cycle.
2019-08-20 | GSE128675 | GEO
Project description:Using ATAC seq analysis, we showed that the MEFs with a knockout of Lmna gene (i.e., missing the lamin A/C nuclear scaffolding protein) (Lmna-/- MEFs) display a striking change in chromatin accessibility landscape (peak signals that are both up and down), both within and outside lamina-associated domains (LADs); moreover, there was a clear overrepresentation of peaks with a gain in chromatin accessibility (within and outside LADs) in the Lmna-/- MEFs, and within LADs compared to outside LADs.
2022-08-31 | GSE186677 | GEO
Project description:The nuclear lamina (NL) is a filamentous layer lining the inner-nuclear-membrane (INM) that aids in the organization of the genome in large domains of low transcriptional activity. Recently, it was shown that the single-cell genome-NL interactions are much more dynamic than previously anticipated, which challenges the concept of the NL as a safe guard for transcriptional repressed genes. Here we discuss the role of the NL in light of these new findings and introduce Lamin A and BAF as potential modulators of LAD positioning BAF-chromatin and Lamin B2-chromatin interactions were assayed in human HT1080 by DamID on Nimblegen microarrays, with two biological replicates each, that were hybridized in a dye-swap design.
2014-02-15 | E-GEOD-55066 | biostudies-arrayexpress
Project description:Senescence is a stress responsive form of stable cell cycle exit. Senescent cells have a distinct gene expression profile, which is often accompanied by the spatial redistribution of heterochromatin into senescence-associated heterochromatic foci (SAHFs). Studying a key component of the nuclear lamina, lamin B1 (LMNB1), we report dynamic alterations in its genomic profile and their implications for SAHF formation and gene regulation during senescence. Genome-wide mapping reveals that LMNB1 is depleted during senescence, preferentially from the central regions of lamina-associated domains (LADs), which are enriched for H3K9me3. LMNB1 knockdown facilitates the spatial relocalization of perinuclear H3K9me3, thus promoting SAHF formation, which is inhibited by ectopic LMNB1 expression. Furthermore, despite the global reduction in LMNB1 protein levels, LMNB1 binding increases during senescence in a small subset of gene-rich regions where H3K27me3 also increases and gene expression becomes repressed. These results suggest that LMNB1 may contribute to senescence in at least two ways due to its uneven genomewide redistribution: firstly through the spatial re-organization of chromatin and, secondly, through gene repression. ChIP-seq for Lamin B1 in Growing and Ras Induced Senescence
2013-08-22 | E-GEOD-49341 | biostudies-arrayexpress
Project description:Interactions of chromatin with the nuclear lamina via lamina-associated domains (LADs) confers structural stability to the genome. The dynamics of positioning of LADs during differentiation, and how LADs impinge on developmental gene expression, remains elusive, however. We examined changes in the association of lamin B1 with the genome in the first 72 hours of differentiation of adipose stem cells into adipocytes. We demonstrate a repositioning of entire stand-alone LADs and of LAD edges as a prominent nuclear structural feature of early adipogenesis. Whereas adipogenic genes are released from LADs, LADs sequester downregulated or repressed genes irrelevant for the adipose lineage. However, LAD repositioning only partly concurs with gene expression changes. Differentially expressed genes in LADs, including LADs conserved throughout differentiation, reside in local euchromatic and lamin-depleted sub-domains. In these sub-domains, pre-differentiation histone modification profiles correlate with the LAD versus inter-LAD outcome of these genes during adipogenic commitment. In addition, differentially expressed genes in LADs are linked to short-range enhancers which overall co-partition with these genes in LADs versus inter-LADs during differentiation. We conclude that LADs are predictable structural features of adipose nuclear architecture that restrain non-adipogenic genes in a repressive environment.
2022-03-21 | GSE185066 | GEO
Project description:Interactions between the nuclear lamina (NL) and chromatin are thought to occur through large lamin association domains (LADs) and correlate with gene repression in these domains. We show that binding of lamin A/C (LMNA) to promoters occurs on discrete domains that are associated with distinct transcriptional outputs. Chromatin immunoprecipitation identifies thousands of LMNA-bound promoters, primarily linked to signaling functions. LMNA often occupies narrow domains on promoters, yet LMNA-bound promoters are often contiguous. LMNA-bound genes are overall repressed, but repression correlates with co-enrichment in repressive histone marks rather than LMNA occupancy per se. Genes marked by LMNA and H3K4me3 escape LMNA-associated repression in the absence of repressive histone marks. Positioning of LMNA on promoters relative to the TSS correlates with distinct transcriptional outputs: whereas upstream-distal binding can be transcriptionally permissive, TSS occupancy is associated with promoter inactivity. Perturbation in NL organization causes reorganization of lamin promoter occupancy and uncouples LMNA binding from promoter inactivity. Our results show the existence of many spatially restricted LMNA binding events on promoter regions, with distinct position-dependent transcriptional outputs. Total RNA obtained from ASCs and ASCs depleted of LMNA (LMNA-KD) and processed for microarray hybridization.
2013-07-14 | E-GEOD-42523 | biostudies-arrayexpress
Project description:Purpose: To compare the interaction of various proteins (in particular Lap2b and Lamin A) at the nuclear periphery with the Lamina Associated Domains (LADs) Results: Using an optimized data analysis workflow (LADetector, available at https://github.com/thereddylab/LADetector), We found near identical sequences within the genome-wide maps indicating that LAP2β and Lamin A, and hence LaminB1, are in close proximity to all LADs, suggesting that these proteins are not involved in discriminating subsets of LADs.
2019-11-01 | GSE128239 | GEO
Project description:The nuclear lamina interacts with the genome through megabase-size lamina-associated domains (LADs). LADs have been identified in proximity labeling assays and recently by chromatin immunoprecipitation-sequencing (ChIP-seq) of A- and B-type lamins. LADs localize mainly to the nuclear periphery, they are gene-poor and largely heterochromatic. Here, we show that the mode of chromatin fragmentation for ChIP, namely either bath sonication (used to date for ChIP of nuclear lamins) or digestion with micrococcal nuclease (MNase) leads to the discovery of distinct sets of lamin-interacting domains (which we refer to as LiDs) with distinct gene content, histone composition enrichment and relationship to lamin B1-interacting domains. We find that total genome coverage by lamin A/C ('LMNA') LiDs identified in sonicated or MNase-digested chromatin is similar (~730 megabases). Over half of these domains, however, are uniquely detected in sonicated or MNase-digested chromatin. Whereas sonication-specific LMNA LiDs are gene-poor and devoid of a broad panel of histone modifications, MNase-specific LMNA LiDs are of higher gene density and are enriched in H3K9me3, H3K27me3 and in histone variant H2A.Z. Analysis of published LMNB1 LADs and of LMNB1 LiDs identified by ChIP-seq further shows that LMNA can associate with 'open' chromatin domains displaying euchromatin features which are not associated with LMNB1. The differential genetic and epigenetic properties of lamin-interacting chromatin domains indicate the existence of distinct LiD populations identifiable in different chromatin contexts, including nuclease-accessible 'open' regions presumably localized in the nuclear interior.
2015-03-24 | GSE57149 | GEO