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Characterization of the Drosophila genome at the nuclear lamina

ABSTRACT: The nuclear lamina (NL) binds chromatin in vitro and is thought to function in its organisation, but genes that interact with the NL are unknown. Using an in vivo approach we identified 474 Drosophila genes that interact with B–type lamin, Lam. These genes are transcriptionally silent, late replicating, lack active histone marks, and are widely spaced. These factors collectively predict Lamin binding behavior, indicating the NL integrates variant and invariant chromatin features. Consistently, NE proximity is partly conserved between cell types and induction of gene expression or active histone marks reduces Lam binding. Lam target genes cluster in the genome, and these clusters are coordinately expressed during development. This genome-wide analysis gives clear insight into the nature and dynamic behavior of the genome at the NL. Keywords: DamID and expression profiling

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE5089 | GEO | 2006/08/29

SECONDARY ACCESSION(S): PRJNA95393

REPOSITORIES: GEO

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Spatially restricted position-dependent implications of lamin A promoter occupancy on gene activity (expression)

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

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Stochastic genome-nuclear lamina interactions: Modulating roles of Lamin A and BAF

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Lamins organize the three dimensional genome from nuclear periphery in ES cells

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Spatially restricted position-dependent implications of lamin A promoter occupancy on gene activity (expression)

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Spatially restricted position-dependent implications of lamin A promoter occupancy on gene activity (ChIPs and MeDips)

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Spatially restricted position-dependent implications of lamin A promoter occupancy on gene activity (ChIPs and MeDips)

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. ChIPs were done from cultured untreated and LMNA-downregulated adipose stem cell (ASC) chromatin. MeDIPs were done from LMNA-downregulated ASCs. ChIP and MeDIP DNA was hybridized onto the aforementioned HG-18 Nimbegen promoter arrays.

2013-07-14 | E-GEOD-42522 | biostudies-arrayexpress

Stochastic genome-nuclear lamina interactions: Modulating roles of Lamin A and BAF

2014-02-15 | GSE55066 | GEO

A-type lamins bind both hetero- and euchromatin, the latter being regulated by lamina-associated polypeptide 2alpha [ChIP-Seq]

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2016-01-19 | E-GEOD-70147 | biostudies-arrayexpress

A-type lamins bind both hetero- and euchromatin, the latter being regulated by lamina-associated polypeptide 2alpha [gene expression]

Project description:Lamins are components of the peripheral nuclear lamina and interact with heterochromatic genomic regions, termed lamina-associated domains (LADs). In contrast to lamin B1, lamin A/C also localizes throughout the nucleus, where it associates with the chromatin-binding protein lamina-associated polypeptide (LAP) 2alpha. Here we show lamin A/C also interacts with euchromatin, as determined by chromatin immunoprecipitation analyses of eu- and heterochromatin-enriched samples. By way of contrast, lamin B1 was only found associated with heterochromatin. Euchromatic regions occupied by lamin A/C overlap with those bound by LAP2alpha, the depletion of which shifts binding of lamin A/C towards more heterochromatic regions. These alterations in lamin A/C chromatin interaction affect epigenetic histone marks in euchromatin without significantly affecting gene expression, while loss of lamin A/C in heterochromatic regions increased gene expression. Our data show a novel role of nucleoplasmic lamin A/C and LAP2alpha in regulating euchromatin. Examination of LaminA, LaminB and Lap2a DNA binding in Lap2alpha +/+ and Lap2a -/- cells and according changes in Histone modifications and gene expression

2016-01-19 | E-GEOD-70148 | biostudies-arrayexpress

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