Baf250A, Brd9 and Baf180 knockdown impact on myoblast transcriptome
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE182421 | GEO | 2022/03/04
REPOSITORIES: GEO
Similar Datasets
Project description:Baf250A, Brd9 and Baf180 knockdown impact on myoblast transcriptome
| PRJNA756240 | ENA
Project description:Copper (Cu)-binding transcription factors are emerging as important regulators of gene expression during skeletal muscle differentiation. Our group has shown that the classic Metal Transcription Factor 1, MTF1, works cooperatively with the myogenic factor MyoD to promote skeletal muscle differentiation and ensure viability of murine primary myoblasts. Preliminary evidence showed that MTF1 interacts with members of the mammalian SWItch/Sucrose Non-Fermentable (mSWI/SNF) family of ATP-dependent chromatin remodeling enzymes to promote differential gene expression in proliferating and differentiating myoblasts. mSWI/SNF complexes are assembled into three major subfamilies that are distinguished by the presence of mutually exclusive subunits: cBAF (canonical BRG1 or BRM-Associated Factor), PBAF (Polybromo containing BAF), or ncBAF (non-canonical BAF). The mechanisms by which each subfamily contributes to the establishment or function of specific cell lineages are poorly understood. We determined the contributions of the BAF, ncBAF, and PBAF complexes to myoblast proliferation, differentiation, and metal homeostasis via knock-down (KD) of a distinguishing subunit of each complex (Baf250A, Brd9, and Baf180, respectively). Biochemical, molecular and RNA-seq analyses showed that Baf250A KD reduced myoblast proliferation rate and differentiation. Brd9 KD resulted in a minor proliferation defect and a delay in myogenesis. KD of Baf180 and other PBAF-specific subunits did not impact proliferation or differentiation but affected the maintenance of metal homeostasis in myoblasts. The data support a model for differential roles and interactions between MTF1 and a novel category of Cu-binding transcription factors and the SWI/SNF enzymes in the development and homeostasis of the skeletal muscle lineage.
2024-10-26 | GSE253377 | GEO
Project description:Copper (Cu)-binding transcription factors are emerging as important regulators of gene expression during skeletal muscle differentiation. Our group has shown that the classic Metal Transcription Factor 1, MTF1, works cooperatively with the myogenic factor MyoD to promote skeletal muscle differentiation and ensure viability of murine primary myoblasts. Preliminary evidence showed that MTF1 interacts with members of the mammalian SWItch/Sucrose Non-Fermentable (mSWI/SNF) family of ATP-dependent chromatin remodeling enzymes to promote differential gene expression in proliferating and differentiating myoblasts. mSWI/SNF complexes are assembled into three major subfamilies that are distinguished by the presence of mutually exclusive subunits: cBAF (canonical BRG1 or BRM-Associated Factor), PBAF (Polybromo containing BAF), or ncBAF (non-canonical BAF). The mechanisms by which each subfamily contributes to the establishment or function of specific cell lineages are poorly understood. We determined the contributions of the BAF, ncBAF, and PBAF complexes to myoblast proliferation, differentiation, and metal homeostasis via knock-down (KD) of a distinguishing subunit of each complex (Baf250A, Brd9, and Baf180, respectively). Biochemical, molecular and RNA-seq analyses showed that Baf250A KD reduced myoblast proliferation rate and differentiation. Brd9 KD resulted in a minor proliferation defect and a delay in myogenesis. KD of Baf180 and other PBAF-specific subunits did not impact proliferation or differentiation but affected the maintenance of metal homeostasis in myoblasts. The data support a model for differential roles and interactions between MTF1 and a novel category of Cu-binding transcription factors and the SWI/SNF enzymes in the development and homeostasis of the skeletal muscle lineage.
2024-10-26 | GSE253376 | GEO
Project description:Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). However, compared to the roles of cBAF, the functions of BRD9/ncBAF in normal and malignant hematopoiesis in vivo have been totally uncharacterized.
2023-10-31 | GSE236960 | GEO
Project description:Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). However, compared to the roles of cBAF, the functions of BRD9/ncBAF in normal and malignant hematopoiesis in vivo have been totally uncharacterized.
2023-10-31 | GSE236326 | GEO
Project description:Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). However, compared to the roles of cBAF, the functions of BRD9/ncBAF in normal and malignant hematopoiesis in vivo have been totally uncharacterized.
2023-10-31 | GSE236327 | GEO
Project description:Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). However, compared to the roles of cBAF, the functions of BRD9/ncBAF in normal and malignant hematopoiesis in vivo have been totally uncharacterized.
2023-11-01 | GSE236959 | GEO
Project description:Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). However, compared to the roles of cBAF, the functions of BRD9/ncBAF in normal and malignant hematopoiesis in vivo have been totally uncharacterized.
2023-10-31 | GSE236330 | GEO
Project description:Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). However, compared to the roles of cBAF, the functions of BRD9/ncBAF in normal and malignant hematopoiesis in vivo have been totally uncharacterized.
2023-10-31 | GSE236328 | GEO
Project description:Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). However, compared to the roles of cBAF, the functions of BRD9/ncBAF in normal and malignant hematopoiesis in vivo have been totally uncharacterized.
2023-11-01 | GSE236958 | GEO