HSPB3 promotes myogenic differentiation by targeting the lamin B receptor.
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ABSTRACT:
PROVIDER: PRJNA671672 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12888377_1.fastq.gz | Fastqsanger.gz | |||
| SRR12888377_2.fastq.gz | Fastqsanger.gz | |||
| SRR12888378_1.fastq.gz | Fastqsanger.gz | |||
| SRR12888378_2.fastq.gz | Fastqsanger.gz | |||
| SRR12888379_1.fastq.gz | Fastqsanger.gz |
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Project description:HSPB3 is a member of the HSPB family that is absent in cycling cells. HSPB3 expression is induced by the myogenic specific transcription factor MyoD in muscle cells, where HSPB3 localizes to the nucleus. Yet, whether HSPB3 participates to muscle cell differentiation is unknown. One of the early events of cell differentiation consists in the switch between the lamin B receptor (LBR) and the lamin A/C (LMNA) tethers, which modulates chromatin remodeling and transcription. Here, we identified LBR as a specialized substrate regulated by HSPB3. HSPB3 affected the expression and nuclear distribution of LBR mimicking the changes that occur during differentiation. HSPB3 upregulation promoted the differentiation of two human muscle cell types: LHCNM2 cells, derived from satellite cells and fusion-negative rhabdomyosarcoma cells, which fail to commit to terminal differentiation. Conversely, HSPB3 depletion stabilized the LBR tether and affected the myogenic transcriptional program. Four mutations in the HSPB3 gene are linked to distal hereditary motor neuropathy and congenital myopathy with unknown mechanisms. We focused on R116P-HSPB3, which was discovered in a myopathy patient with chromatin alterations and muscle fiber disorganization. Upon overexpression in cells R116-HSPB3 formed nuclear aggregates that immobilized LBR-GFP. In LHCNM2 cells R116-HSPB3 deregulated the transcriptional program required for cytoskeleton and ECM remodeling, while activating the unfolded protein response. We propose that HSPB3 is a highly specialized chaperone that participates to muscle cell differentiation by targeting LBR. Our findings pave the way for a better understanding of HSPB3 implication in the physiology and pathology of the neuromuscular system.
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Project description:Calcineurin promotes myogenic gene expression
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2013-01-28 | E-GEOD-37076 | biostudies-arrayexpress
Project description:influence of lamin B rereceptor knockout and lamin A/C knockout on gene expression in cultured myoblast cells and in striated muscle tissue
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Project description:While skeletal myogenesis is tightly coordinated by myogenic regulatory factors including MyoD and myogenin, chromatin modifications have emerged as vital mechanisms of myogenic regulation. We have previously established that bexarotene, a clinically approved agonist of retinoid X receptor, promotes the specification and differentiation of skeletal muscle lineage. Here, we examine a genome-wide impact of rexinoids on myogenic differentiation through integral RNA-seq and ChIP-seq analyses. We found that bexarotene promotes myoblast differentiation through the coordination of exit from the cell cycle and the activation of muscle-related genes. We uncovered a new mechanism of rexinoid action which is mediated by the nuclear receptor and largely reconciled through a direct regulation of MyoD gene expression. In addition, we determined a rexinoid-responsive residue-specific histone acetylation at a distinct chromatin state associated to MyoD and myogenin. Thus, we provide novel molecular insights into the interplay between retinoid X receptor signaling and chromatin states pertinent to myogenic programs in early myoblast differentiation.
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Project description:Gene positioning and regulation of nuclear architecture are thought to influence gene expression. Here, we show that in mouse olfactory neurons, silent olfactory receptor (OR) genes from different chromosomes converge in a small number of heterochromatic foci. These foci are OR-exclusive and form in a cell-type-specific and differentiation- dependent manner. The aggregation of OR genes is developmentally synchronous with the downregulation of Lamin b Receptor (LBR) and can be reversed by ectopic expression of LBR in mature olfactory neurons. LBR-induced reorganization of nuclear architecture and redistribution of OR loci results in misregulation of OR transcription and disruption of the targeting specificity of the olfactory neurons. Our observations are consistent with a model of spatial regulation of OR expression and provide evidence for the instructive role of nuclear architecture and compartmentalization in gene regulation and differentiation. A complex probe was made by array capture to label mouse olfactory receptor genes by DNA FISH; this microarray data verifies the composition of that probe. Probe was made by array capture and elution from a custom olfactory receptor genomic region tiling array. Probe was verified on a chr1-4 tiling array.
2012-08-30 | E-GEOD-38488 | biostudies-arrayexpress
Project description:A-type lamins form a filamentous meshwork beneath the nuclear membrane that anchors large heterochromatic chromatin domains at the nuclear envelope. They also exist as a more dynamic, non-filamentous pool in the nuclear interior, where they interact with gene-rich euchromatin. Lamin-associated polypeptide 2 alpha (LAP2alpha) binds to and maintains the nucleoplasmic lamin pool, but the functional significance of this interaction is poorly understood. Here we investigate the genome-wide chromatin association of A-type lamins during myogenic differentiation in the presence and absence of LAP2alpha. We find that A-type lamins are significantly reorganized on chromatin upon depletion of LAP2alpha, spreading towards active chromatin and accumulating at regions of active H3K27ac and H3K4me3 histone marks close to the genes whose expression is impaired in the absence of LAP2alpha. This reorganization of A-type lamins on chromatin is accompanied by depletion of the active chromatin mark H3K27ac and a significant delay of myogenic differentiation. Thus, the interplay of lamins and LAP2alpha is crucial for proper positioning of intranuclear lamins on chromatin to allow normal myogenic differentiation. This research was funded in whole or in part by the Austrian Science Fund (FWF) to Roland Foisner: P32512-B/DOI:10.55776/P36503 https://www.doi.org/10.55776/P36503 P36503-B/DOI:10.55776/P32512 https://www.doi.org/10.55776/P32512
2024-08-08 | GSE247771 | GEO
Project description:A-type lamins form a filamentous meshwork beneath the nuclear membrane that anchors large heterochromatic chromatin domains at the nuclear envelope. They also exist as a more dynamic, non-filamentous pool in the nuclear interior, where they interact with gene-rich euchromatin. Lamin-associated polypeptide 2 alpha (LAP2alpha) binds to and maintains the nucleoplasmic lamin pool, but the functional significance of this interaction is poorly understood. Here we investigate the genome-wide chromatin association of A-type lamins during myogenic differentiation in the presence and absence of LAP2alpha. We find that A-type lamins are significantly reorganized on chromatin upon depletion of LAP2alpha, spreading towards active chromatin and accumulating at regions of active H3K27ac and H3K4me3 histone marks close to the genes whose expression is impaired in the absence of LAP2alpha. This reorganization of A-type lamins on chromatin is accompanied by depletion of the active chromatin mark H3K27ac and a significant delay of myogenic differentiation. Thus, the interplay of lamins and LAP2alpha is crucial for proper positioning of intranuclear lamins on chromatin to allow normal myogenic differentiation. This research was funded in whole or in part by the Austrian Science Fund (FWF) to Roland Foisner: P32512-B/DOI:10.55776/P36503 https://www.doi.org/10.55776/P36503 P36503-B/DOI:10.55776/P32512 https://www.doi.org/10.55776/P32512
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