ArticleGenome biology2014
Genome-wide analysis links emerin to neuromuscular junction activity in Caenorhabditis elegans.
Article in Genome biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 58 citations in OpenAlex.
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- Nuclear envelope assembly relies on CHMP-7 in the absence of BAF-LEM-mediated hole closure.Journal of cell science · 2023Article
- Nuclear envelope assembly relies on CHMP-7 in the absence of BAF-LEM-mediated hole closure.bioRxiv : the preprint server for biology · 2023Article
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- Drosophila female germline stem cells undergo mitosis without nuclear breakdown.Current biology : CB · 2021Article
- Survival ofDevelopment (Cambridge, England) · 2020Article
- Loss of an H3K9me anchor rescues laminopathy-linked changes in nuclear organization and muscle function in an Emery-Dreifuss muscular dystrophy model.Genes & development · 2020Article
- Transcription-independent TFIIIC-bound sites cluster near heterochromatin boundaries within lamina-associated domains in C. elegans.Epigenetics & chromatin · 2020Article
- Active chromatin marks drive spatial sequestration of heterochromatin in C. elegans nuclei.Nature · 2019Article
- Optimization of DamID for use in primary cultures of mouse hepatocytes.Methods (San Diego, Calif.) · 2019Article
- The large fraction of heterochromatin in Drosophila neurons is bound by both B-type lamin and HP1a.Epigenetics & chromatin · 2018Article
- Nuclear lamina dysfunction triggers a germline stem cell checkpoint.Nature communications · 2018Article
- Repressive Chromatin inGenetics · 2018Review
- Article
- Lamina-Associated Domains: Links with Chromosome Architecture, Heterochromatin, and Gene Repression.Cell · 2017Review
- Cell Biology of the Caenorhabditis elegans Nucleus.Genetics · 2017Review
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundLaminopathies are diseases characterized by defects in nuclear envelope structure. A well-known example is Emery-Dreifuss muscular dystrophy, which is caused by mutations in the human lamin A/C and emerin genes. While most nuclear envelope proteins are ubiquitously expressed, laminopathies often affect only a subset of tissues. The molecular mechanisms underlying these tissue-specific manifestations remain elusive. We hypothesize that different functional subclasses of genes might be differentially affected by defects in specific nuclear envelope components.
resultsHere we determine genome-wide DNA association profiles of two nuclear envelope components, lamin/LMN-1 and emerin/EMR-1 in adult Caenorhabditis elegans. Although both proteins bind to transcriptionally inactive regions of the genome, EMR-1 is enriched at genes involved in muscle and neuronal function. Deletion of either EMR-1 or LEM-2, another integral envelope protein, causes local changes in nuclear architecture as evidenced by altered association between DNA and LMN-1. Transcriptome analyses reveal that EMR-1 and LEM-2 are associated with gene repression, particularly of genes implicated in muscle and nervous system function. We demonstrate that emr-1, but not lem-2, mutants are sensitive to the cholinesterase inhibitor aldicarb, indicating altered activity at neuromuscular junctions.
conclusionsWe identify a class of elements that bind EMR-1 but do not associate with LMN-1, and these are enriched for muscle and neuronal genes. Our data support a redundant function of EMR-1 and LEM-2 in chromatin anchoring to the nuclear envelope and gene repression. We demonstrate a specific role of EMR-1 in neuromuscular junction activity that may contribute to Emery-Dreifuss muscular dystrophy in humans.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.