Drosophila Myb-MuvB/dREAM
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE9088E-GEOD-8751
PROVIDER: PRJNA102609 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Myb-MuvB (MMB)/dREAM is a nine subunit complex first described in Drosophila as a repressor of transcription, dependent upon E2F2 and the RBFs. Myb, an integral member of MMB, curiously plays no role in the silencing of the test genes previously analyzed. Moreover, Myb plays an activating role in DNA replication in Drosophila egg chamber follicle cells. The essential functions for Myb are executed as part of MMB. This duality of function lead to the hypothesis that MMB, which contains both known activator and repressor proteins, might function as part of a switching mechanism that is dependent upon DNA sites and developmental context. Keywords: Drosophila Myb-MuvB/dREAM, ChIP-chip
2007-11-14 | GSE9087 | GEO
Project description:Myb-MuvB (MMB)/dREAM is a nine subunit complex first described in Drosophila as a repressor of transcription, dependent upon E2F2 and the RBFs. Myb, an integral member of MMB, curiously plays no role in the silencing of the test genes previously analyzed. Moreover, Myb plays an activating role in DNA replication in Drosophila egg chamber follicle cells. The essential functions for Myb are executed as part of MMB. This duality of function lead to the hypothesis that MMB, which contains both known activator and repressor proteins, might function as part of a switching mechanism that is dependent upon DNA sites and developmental context. Here, we used proliferating Drosophila Kc tissue culture cells to explore both the network of genes regulated by MMB (employing RNAi and micro-array expression analysis) and the genomic locations of MMB following chromatin immunoprecipitation (ChIP) and tiling array analysis. MMB occupies thousands of chromosomal sites where a substantial number are proximal to repressed genes that are normally expressed in a wide range of developmental pathways. At many of these sites, E2F2 was critical for repression whereas at other non-overlapping sites, Myb was critical for repression. These data highlight that the MMB factors are utilized in a combinatorial way for targeting gene regulation. We also found sites where MMB was a positive regulator of transcript levels that included genes required for mitotic functions (G2/M), which may explain some of the chromosome instability phenotypes attributed to loss of Myb function in myb mutants. Keywords: Drosophila Myb-MuvB/dREAM, RNAi, ChIP-chip
2007-11-14 | GSE8751 | GEO
Project description:Myb-MuvB (MMB)/dREAM is a nine subunit complex first described in Drosophila as a repressor of transcription, dependent upon E2F2 and the RBFs. Myb, an integral member of MMB, curiously plays no role in the silencing of the test genes previously analyzed. Moreover, Myb plays an activating role in DNA replication in Drosophila egg chamber follicle cells. The essential functions for Myb are executed as part of MMB. This duality of function lead to the hypothesis that MMB, which contains both known activator and repressor proteins, might function as part of a switching mechanism that is dependent upon DNA sites and developmental context. Here, we used proliferating Drosophila Kc tissue culture cells to explore both the network of genes regulated by MMB (employing RNAi and micro-array expression analysis) and the genomic locations of MMB following chromatin immunoprecipitation (ChIP) and tiling array analysis. MMB occupies thousands of chromosomal sites where a substantial number are proximal to repressed genes that are normally expressed in a wide range of developmental pathways. At many of these sites, E2F2 was critical for repression whereas at other non-overlapping sites, Myb was critical for repression. These data highlight that the MMB factors are utilized in a combinatorial way for targeting gene regulation. We also found sites where MMB was a positive regulator of transcript levels that included genes required for mitotic functions (G2/M), which may explain some of the chromosome instability phenotypes attributed to loss of Myb function in myb mutants. Experiment Overall Design: RNAi to deplete Lin-52, Mip40, Myb, Mip120, Mip130, E2F2, both RBFs (RBF1 and RBF2) and L(3)MBT were performed in triplicate. RNAi with a nonspecific RNA derived from a pBSK+ plasmid (named SK+) was used as control. Total RNA was extracted from RNAi-transfected cells after 4 days using RNeasy Mini Kit (QIAGEN).
2008-06-16 | E-GEOD-8751 | biostudies-arrayexpress
Project description:Drosophila Myb-MuvB/dREAM (Expression data)
| PRJNA105291 | ENA
Project description:Drosophila Myb-MuvB/dREAM (ChIP-chip data)
| PRJNA105213 | ENA
Project description:To identify genomic regions bound by B-Myb and LIN9 (a subunit of the MuvB complex), we performed ChIP-Sequencing (ChIP-Seq) using chromatin from proliferating HeLa cells in which we can detect a robust association between B-Myb and subunits of the MuvB complex. This analysis allowed us identify late cell cycle or G2/M expressed genes as specific targets of the B-Myb-MuvB complex. Examination of B-Myb and LIN9 binding in asynchronously growing HeLa cells
2012-01-25 | E-GEOD-27030 | biostudies-arrayexpress
Project description:The highly conserved DREAM transcriptional repressor complex contains an RB-like pocket protein, an E2F-DP transcription factor heterodimer, and the 5-subunit MuvB complex. Using CRISPR/Cas9 targeted mutagenesis, we disrupted the interaction between the sole Caenorhabditis elegans pocket protein LIN-35 and the MuvB subunit LIN-52. A triple alanine substitution of LIN-52's LxCxE motif (3A) severed LIN-35-MuvB association and caused classical DREAM mutant phenotypes, including synthetic multiple vulvae, high-temperature arrest, and ectopic expression of germline genes in the soma. We performed RNA-seq in lin-52(3A) mutant late embryos (4 replicates) compared to lin-52(WT) wild-type late embryos (4 replicates) to assess the genome-wide effects on gene expression that result from severing LIN-35-MuvB association.
2022-05-24 | GSE199287 | GEO
Project description:A-MYB (MYBL1) is a transcription factor with a role in meiosis in spermatocytes. The related B-MYB protein is a key proto-oncogene and a master regulator activating late cell cycle genes. To activate genes, B-MYB forms a complex with MuvB and is recruited indirectly to cell cycle genes homology region (CHR) promoter sites of target genes. Activation through the B-MYB-MuvB (MMB) complex is essential for successful mitosis. Here, we discover that A-MYB has a function in transcriptional regulation of the mitotic cell cycle and can substitute for B-MYB. Knockdown experiments in cells not related to spermatogenesis show that B-MYB loss alone only delays cell cycle progression. Only dual knockdown of B-MYB and A-MYB causes cell cycle arrest. A-MYB can substitute for B-MYB in binding to MuvB. The resulting A-MYB-MuvB complex activates genes through CHR sites. We find that A-MYB activates the same target genes as B-MYB. Many of the corresponding proteins are central regulators of the cell division cycle. In summary, we demonstrate that A-MYB is an activator of the mitotic cell cycle by activating late cell cycle genes.
2024-02-29 | GSE240799 | GEO
Project description:The core cell cycle machinery genes are transcriptionally regulated by the MuvB family of protein complexes in a cell cycle specific manner. During cell cycle exit in quiescence or senescence, the DREAM complex, which is the repressive form of MuvB, directs transcriptional repression of cell cycle genes; conversely during cell proliferation, the complex of MuvB with the transcription factors (TFs) B-MYB and FOXM1 activate mitotic genes during the G2 phase of the cell cycle. The mechanisms of transcriptional regulation of these complexes are still poorly characterised. Here we combine biochemical analysis and in vitro reconstitution, with structural analysis by cryo-electron microscopy (cryo-EM) and cross-linking mass spectrometry (XL-MS), to functionally examine these complexes. Our data suggests that MuvB is a chromatin regulator whereby a core region binds the nucleosome and remodels it, thereby exposing nucleosomal DNA. This remodelling activity is supported by B-MYB which directly binds the remodelled DNA. Given the remodelling activity on the nucleosome, we propose that the MuvB complex with B-MYB (MMB) function as a pioneer transcription factor complex. Our data rationalises prior biochemical and cellular studies and provides a molecular framework of interactions on a protein complex, which is key for cell cycle regulation.
2022-08-17 | PXD031421 | Pride
Project description:The mammalian Retinoblastoma (RB) family including pRB, p107, and p130 represses E2F target genes through mechanisms that are not fully understood. In D. melanogaster, RB-dependent repression is mediated in part by the multisubunit protein complex Drosophila RBF, E2F, and Myb (dREAM) that contains homologs of the C. elegans synthetic multivulva class B (synMuvB) gene products. Using an integrated approach combining proteomics, genomics, and bioinformatic analyses, we identified a p130 complex termed DP, RB-like, E2F, and MuvB (DREAM) that contains mammalian homologs of synMuvB proteins LIN-9, LIN-37, LIN-52, LIN-54, and LIN-53/RBBP4. DREAM bound to more than 800 human promoters in G0 and was required for repression of E2F target genes. In S phase, MuvB proteins dissociated from p130 and formed a distinct submodule that bound MYB. This work reveals an evolutionarily conserved multisubunit protein complex that contains p130 and E2F4, but not pRB, and mediates the repression of cell cycle-dependent genes in quiescence. Experiment Overall Design: Gene expression during the cell cycle in T98G cells. Cells were serum starved for 72 hours to induce G0 and then restimuated to enter cell cycle by serum addition. BrdU and FACS was done simultaneously to confirm their cell cycle phase.
2008-06-16 | E-GEOD-8537 | biostudies-arrayexpress