Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA196425 | ENA |
REPOSITORIES: ENA
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Project description:Precise control of gene expression during differentiation relies on the interplay of chromatin and nuclear structure. Despite an established contribution of nuclear membrane proteins to developmental gene regulation, little is known regarding the role of inner nuclear proteins. Here we demonstrate that loss of the nuclear scaffolding protein Matrin-3 (Matr3) in erythroid cells leads to morphological and gene expression changes characteristic of accelerated maturation, as well as broad alterations in chromatin organization similar to those accompanying differentiation. Matr3 protein interacts with CTCF and the cohesin complex, and its loss perturbs their occupancy at a subset of sites. Destabilization of CTCF and cohesin binding correlates with altered transcription and accelerated differentiation. This association is conserved in embryonic stem cells. Our findings indicate Matr3 negatively affects cell fate transitions and demonstrate that a critical inner nuclear protein impacts occupancy of architectural factors, culminating in broad effects on chromatin organization and cell differentiation.
2021-11-11 | PXD028867 | Pride
Project description:Cell differentiation is based on a synchronised orchestra of complex pathways of intrinsic and extrinsic signals that manifest in the induced expression of specific transcription factors and pivotal genes within the nucleus. One cannot ignore the epigenetic status of differentiating cells, comprising not only histones and DNA modifications but also the spatial and temporal intranuclear chromatin organisation, which is an important regulator of nuclear processes. In the present study, we investigated the nuclear architecture of human primary myoblasts and myocytes in an in vitro culture, with reference to global changes in genomic expression. Repositioning of the chromosomal centromeres, along with alterations in the nuclear shape and volume, was observed as a consequence of myotube formation. Moreover, the microarray data showed that during in vitro myogenesis cells tend to silence rather than induce gene expression. The creation of a chromosome map marked with gene expression changes that were at least 2-fold confirmed the observation. Additionally, almost all of the chromosomal centromeres in the differentiated cells preferentially localised near the nuclear periphery when compared to the undifferentiated cells. The exceptions were chromosomes 7 and 11, in which we were unable to confirm the centromere repositioning. In our opinion, this is the first reported observation of the movement of chromosomal centromeres along differentiating myogenic cells. Based on these data we can conclude that the myogenic differentiation with global gene expression changes is accompanied by the spatial repositioning of chromosomes and chromatin remodelling, which are important processes that regulate cell differentiation. Six samples from human skeletal muscle stem cells populations before and after differentiation were analysed
2013-04-06 | E-GEOD-45819 | biostudies-arrayexpress
Project description:DNA methylation analysis during in vitro myogenic differentiation
| PRJNA240072 | ENA
Project description:Mitochondrial dysfunction caused by mitochondrial DNA (mtDNA) damage has been associated with the progressive decline of multiple tissues during aging. Muscle satellite cells (MuSCs), which sustain skeletal muscle regeneration throughout life, exhibit reduced number and regenerative capacity with age. Yet, the contribution of mtDNA mutations to MuSC integrity and their impact on skeletal muscle remain poorly understood. Here, we used a dominant-negative variant of the mitochondrial helicase Twinkle (K320E) to induce mtDNA alterations in C2C12 myoblasts and MuSCs and investigated myogenic differentiation. During C2C12 differentiation, impaired mtDNA integrity disrupted respiratory complex assembly, increased reactive oxygen species, and directly compromised proper differentiation. Proximity proteomics in C2C12 differentiated cells revealed that K320E expression not only affects mtDNA encoded proteins, but also reshapes the complete mitochondrial proteome. In vivo, using the fluorescent reporter mitoTIMER, we found that mtDNA alterations in MuSCs, increased mitochondrial oxidation at early stages of differentiation, which normalized at later stages. Finally, by mimicking the age-dependent accumulation of mtDNA alterations, we show that mtDNA defects in MuSCs are transmitted to mature skeletal muscle. These defects induced architectural changes in muscle, including a glycolytic-to-oxidative fiber type transition reminiscent of aging human muscle. Together, our results establish a mechanistic link between mtDNA instability in muscle progenitors and aging of the skeletal muscle. With these results, we demonstrate that alterations in the mtDNA of muscle progenitors are sufficient to drive long-term changes in muscle architecture that may contribute to age-dependent functional decline.
2026-08-17 | PXD073846 | Pride
Project description:During myogenic differentiation the architecture and proteome of muscle stem cells undergo extensive remodelling. These processes are only partially understood and display impairments in age and disease. Using mass spectrometry to analyse protein dynamics during myogenic differentiation, we identified the actin nucleator Leiomodin 1 (LMOD1) increasing in abundance in early phases of myogenic differentiation. Knockdown of LMOD1 in primary myoblasts severely affected myogenic differentiation and fusion of myotubes, while overexpression had the opposite effect. Mechanistically, we show that LMOD1 interacts with Sirtuin1 (SIRT1) and that both follow similar changes in nuclear/cytoplasmic localization during differentiation. We demonstrate that LMOD1 influences SIRT1 localization and the expression of a subset of its target genes. Consistently, depletion or pharmacological inhibition of SIRT1 partially rescues the effects of LMOD1 knockdown. Our work identifies a novel regulator of myogenic differentiation that might be a potential target to improve muscle regeneration in aging and disease.
2024-08-31 | GSE254443 | GEO
Project description:Precise control of gene expression during differentiation relies on the interplay of chromatin and nuclear structure. Despite an established contribution of nuclear membrane proteins to developmental gene regulation, little is known regarding the role of inner nuclear proteins. Here we demonstrate that loss of the nuclear scaffolding protein Matrin-3 (Matr3) in erythroid cells leads to morphological and gene expression changes characteristic of accelerated maturation, as well as broad alterations in chromatin organization similar to those accompanying differentiation. Matr3 protein interacts with CTCF and the cohesin complex, and its loss perturbs their occupancy at a subset of sites. Destabilization of CTCF and cohesin binding correlates with altered transcription and accelerated differentiation. This association is conserved in embryonic stem cells. Our findings indicate Matr3 negatively affects cell fate transitions and demonstrate that a critical inner nuclear protein impacts occupancy of architectural factors, culminating in broad effects on chromatin organization and cell differentiation.
2021-09-20 | GSE181233 | GEO
Project description:Precise control of gene expression during differentiation relies on the interplay of chromatin and nuclear structure. Despite an established contribution of nuclear membrane proteins to developmental gene regulation, little is known regarding the role of inner nuclear proteins. Here we demonstrate that loss of the nuclear scaffolding protein Matrin-3 (Matr3) in erythroid cells leads to morphological and gene expression changes characteristic of accelerated maturation, as well as broad alterations in chromatin organization similar to those accompanying differentiation. Matr3 protein interacts with CTCF and the cohesin complex, and its loss perturbs their occupancy at a subset of sites. Destabilization of CTCF and cohesin binding correlates with altered transcription and accelerated differentiation. This association is conserved in embryonic stem cells. Our findings indicate Matr3 negatively affects cell fate transitions and demonstrate that a critical inner nuclear protein impacts occupancy of architectural factors, culminating in broad effects on chromatin organization and cell differentiation.
2021-09-20 | GSE181232 | GEO
Project description:Precise control of gene expression during differentiation relies on the interplay of chromatin and nuclear structure. Despite an established contribution of nuclear membrane proteins to developmental gene regulation, little is known regarding the role of inner nuclear proteins. Here we demonstrate that loss of the nuclear scaffolding protein Matrin-3 (Matr3) in erythroid cells leads to morphological and gene expression changes characteristic of accelerated maturation, as well as broad alterations in chromatin organization similar to those accompanying differentiation. Matr3 protein interacts with CTCF and the cohesin complex, and its loss perturbs their occupancy at a subset of sites. Destabilization of CTCF and cohesin binding correlates with altered transcription and accelerated differentiation. This association is conserved in embryonic stem cells. Our findings indicate Matr3 negatively affects cell fate transitions and demonstrate that a critical inner nuclear protein impacts occupancy of architectural factors, culminating in broad effects on chromatin organization and cell differentiation.
2021-09-20 | GSE181231 | GEO
Project description:Precise control of gene expression during differentiation relies on the interplay of chromatin and nuclear structure. Despite an established contribution of nuclear membrane proteins to developmental gene regulation, little is known regarding the role of inner nuclear proteins. Here we demonstrate that loss of the nuclear scaffolding protein Matrin-3 (Matr3) in erythroid cells leads to morphological and gene expression changes characteristic of accelerated maturation, as well as broad alterations in chromatin organization similar to those accompanying differentiation. Matr3 protein interacts with CTCF and the cohesin complex, and its loss perturbs their occupancy at a subset of sites. Destabilization of CTCF and cohesin binding correlates with altered transcription and accelerated differentiation. This association is conserved in embryonic stem cells. Our findings indicate Matr3 negatively affects cell fate transitions and demonstrate that a critical inner nuclear protein impacts occupancy of architectural factors, culminating in broad effects on chromatin organization and cell differentiation.
2021-09-20 | GSE181230 | GEO
Project description:Porcine muscle-derived stem cells hold significant potential as a resource for both cellular agriculture and regenerative medicine. In this study, stem cells were isolated from porcine skeletal muscle tissue and cultured in vitro to investigate their transcriptional profiles using bulk RNA sequencing. This transcriptomic analysis provided an overview of gene expression changes during myogenic differentiation under culture conditions. The results revealed dynamic shifts in gene expression patterns over time and identified key regulatory genes associated with various stages of myogenic commitment. These findings contribute to a deeper understanding of stem cell behavior in vitro and offer valuable data for optimizing expansion and differentiation protocols.
2026-06-18 | GSE293835 | GEO