HDAC4 regulates satellite cell proliferation and differentiation by targeting P21 and Sharp1 genes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA417021 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6246160.fastq.gz | Fastqsanger.gz | |||
| SRR6246161.fastq.gz | Fastqsanger.gz | |||
| SRR6246162.fastq.gz | Fastqsanger.gz | |||
| SRR6246163.fastq.gz | Fastqsanger.gz | |||
| SRR6246164.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:NGS technology was used for high-throughput profiling of the transcriptome by comparing satellite cells lacking or not HDAC4.
2018-02-28 | GSE106445 | GEO
Project description:Skeletal muscle exhibits a high regenerative capacity, mainly due to the ability of satellite cells to replicate and differentiate in response to appropriate stimuli. Epigenetic control is effective at different stages of this process. It has been shown that the chromatin-remodeling factor HDAC4 is able to regulate satellite cell proliferation and commitment. However, its molecular targets are still uncovered. To explain the signaling pathways regulated by HDAC4 in satellite cells, we generated tamoxifen-inducible mice with conditional inactivation of HDAC4 in Pax7+ cells (HDAC4 KO mice). We found that the proliferation and differentiation of HDAC4 KO satellite cells were compromised, although similar amounts of satellite cells were found in mice. Moreover, we found that the inhibition of HDAC4 in satellite cells was sufficient to block the differentiation process. By RNA-sequencing analysis we identified P21 and Sharp1 as HDAC4 target genes. Reducing the expression of these target genes in HDAC4 KO satellite cells, we also defined the molecular pathways regulated by HDAC4 in the epigenetic control of satellite cell expansion and fusion.
| S-EPMC5823886 | biostudies-literature
Project description:Craniofacial development involves regulation of a compendium of transcription factors, signaling molecules and epigenetic regulators. Histone deacetylases (HDACs) are involved in the regulation of cell proliferation, differentiation and homeostasis across a wide range of tissues, such as brain, cardiovascular system, muscular system, and skeletal system. However, functional role of Hdac4 during craniofacial development is still unclear. In this study, we investigated the effects of Hdac4 knockout in craniofacial skeletal development by conditionally disrupting the Hdac4 gene in cranial neural crest cells (CNCCs) using Cre-mediated recombination. Mice deficient in Hdac4 in CNCCs-derived osteoblasts demonstrated a dramatic decrease in bone formation in frontal bone. In vitro pre-osteoblasts (MC3T3-E1 cells) lacking Hdac4 exhibited reduced proliferation activity in association with dysregulation of cell cycle-related genes. These findings suggest that Hdac4 acts partially as a regulator of craniofacial skeletal development by positively regulating proliferation of CNCCs-derived osteoblasts.
2022-03-09 | GSE186707 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2018-02-28 | GSE106485 | GEO
Project description:DDB1-cullin-4-associated factor-2 (DCAF2, also known as DTL or CDT2), a conserved substrate recognition protein of Cullin-RING E3 ligase 4 (CRL4), recognises and degrades several substrate proteins during the S phase to maintain cell cycle progression and genome stability. Our study found that Dcaf2 was highly expressed in the germ cells of human and mouse testes. To determine whether DCAF2 plays a crucial role in spermatogenesis, we generated germ cell conditional Dcaf2 knockout mice by crossing Dcaf2fl/fl mice with Stra8-Cre mice. The depletion of Dcaf2 in germ cells causes a reduction in progenitor spermatogonia and differentiating spermatogonia, eventually leading to the failure of meiosis initiation and male infertility. Further study showed that depletion of Dcaf2 in germ cells caused abnormal accumulation of the substrate proteins cyclin-dependent kinase inhibitor 1A (p21) and thymine DNA glycosylase (TDG). Overexpression of p21 or TDG attenuates proliferation and increases DNA damage and apoptosis in GC-1 cells. Co-overexpression of p21 and TDG exacerbates DNA damage and apoptosis. These results suggest that DCAF2 maintains the expansion and differentiation of progenitor spermatogonia by targeting the substrate proteins p21 and TDG.
2024-05-01 | GSE259242 | GEO
Project description:Transcriptome analysis of satellite cells with a genetic deletion of HDAC4 to identify the gene modulated by HDAC4
| PRJNA416903 | ENA
Project description:In this study, we directly compared turkey muscle satellite cell gene expression between satellite cells with the gene Matrix Gla Protein (MGP) knocked down by siRNA transfection and those transfected with a lipofectamine control using our 6K Turkey Skeletal Muscle Long Oligo (TSKMLO) microarray (GPL9788). The MGP gene was previously identified as differentially expressed by genetic line and during development of turkey skeletal muscle (Sporer et al., 2011). Gene expression changes were investigated in satellite cells after 72 h of proliferation and after 48 h of differentiation. We identified novel candidate genes and pathways as playing potentially crucial roles in the MGP-mediated effects on the normal processes of proliferation and differentiation in turkey satellite cells previously identified by Velleman et al. (submitted). This experiment was designed to investigate the role of MGP expression in turkey satellite cells during two crucial processes in muscle development: proliferation and differentiation. Satellite cells were isolated from 7-week-old turkeys from the RBC2 line. Cells were transfected with either MGP siRNA or a lipofectamine control; MGP expression was knocked down by over 50% with siRNA transfection (Velleman et al., submitted). Satellite cells were then induced to proliferate for 72h or differentiate for 48h; culture plates from each stage (n=4) were frozen until RNA extraction. Microarrays directly compared the MGP -knockdown to control from each of 4 culture plates and utilized a dye swap to equal 8 arrays for each of the cell developmental stages, proliferation and differentiation, and 16 arrays for the overall experiment investigating the role of MGP expression in satellite cell development and function. Hybridizations were performed in random order.
2012-05-31 | E-GEOD-36362 | biostudies-arrayexpress
Project description:In this study, we directly compared turkey muscle satellite cell gene expression between satellite cells with the gene versican (VCAN) knocked down by siRNA transfection and those transfected with a lipofectamine control using our 6K Turkey Skeletal Muscle Long Oligo (TSKMLO) microarray (GPL9788). The VCAN gene was previously identified as differentially expressed by genetic line and during development of turkey skeletal muscle (Sporer et al., 2011). Gene expression changes were investigated in satellite cells after 72 h of proliferation and after 48 h of differentiation. We identified novel candidate genes and pathways as playing potentially crucial roles in the VCAN-mediated effects on the normal processes of proliferation and differentiation in turkey satellite cells previously identified by Velleman et al. (submitted). This experiment was designed to investigate the role of VCAN expression in turkey satellite cells during two crucial processes in muscle development: proliferation and differentiation. Satellite cells were isolated from 7-week-old turkeys from the RBC2 line. Cells were transfected with either VCAN siRNA or a lipofectamine control; VCAN expression was knocked down by over 50% with siRNA transfection (Velleman et al., submitted). Satellite cells were then induced to proliferate for 72h or differentiate for 48h; culture plates from each stage (n=4) were frozen until RNA extraction. Microarrays directly compared the VCAN-knockdown to control from each of 4 culture plates and utilized a dye swap to equal 8 arrays for each of the cell developmental stages, proliferation and differentiation, and 16 arrays for the overall experiment investigating the role of VCAN expression in satellite cell development and function. Hybridizations were performed in random order.
2012-05-31 | E-GEOD-36365 | biostudies-arrayexpress
Project description:In this study, we directly compared turkey muscle satellite cell gene expression between satellite cells with the gene Death-Associated Protein (DAP) knocked down by siRNA transfection and those transfected with a lipofectamine control using our 6K Turkey Skeletal Muscle Long Oligo (TSKMLO) microarray (GPL9788). The DAP gene was previously identified as differentially expressed by genetic line and during development of turkey skeletal muscle (Sporer et al., 2011). Gene expression changes were investigated in satellite cells after 72 h of proliferation and after 48 h of differentiation. We identified novel candidate genes and pathways as playing potentially crucial roles in the DAP-mediated attenuation of the normal processes of proliferation and differentiation in turkey satellite cells previously identified by Velleman et al. (submitted). This experiment was designed to investigate the role of DAP expression in turkey satellite cells during two crucial processes in muscle development: proliferation and differentiation. Satellite cells were isolated from 7-week-old turkeys from the RBC2 line. Cells were transfected with either DAP siRNA or a lipofectamine control; DAP expression was knocked down by over 50% with siRNA transfection (Velleman et al., submitted). Satellite cells were then induced to proliferate for 72h or differentiate for 48h; culture plates from each stage (n=4) were frozen until RNA extraction. Microarrays directly compared the DAP-knockdown to control from each of 4 culture plates and utilized a dye swap to equal 8 arrays for each of the cell developmental stages, proliferation and differentiation, and 16 arrays for the overall experiment investigating the role of DAP expression in satellite cell development and function. Hybridizations were performed in random order.
2012-05-31 | E-GEOD-35660 | biostudies-arrayexpress
Project description:Hdac4 has been found to modulate symptoms in Huntington's Disease (HD) mouse models through an uknown mechanism unrelated to any enzymatic activity. We investigated the protein-protein interactions to gain insight into the role of Hdac4 in HD.
2019-05-01 | PXD011845 | Pride