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Results: 1 to 4 of 4

Publication Record


ETO family protein Mtg16 regulates the balance of dendritic cell subsets by repressing Id2.
Ghosh HS, Ceribelli M, Matos I, Lazarovici A, Bussemaker HJ, Lasorella A, Hiebert SW, Liu K, Staudt LM, Reizis B
(2014) J Exp Med 211: 1623-35
MeSH Terms: Animals, Base Sequence, Cell Differentiation, Cell Line, Cell Proliferation, Chromatin, Dendritic Cells, E2F2 Transcription Factor, Gene Deletion, Humans, Inhibitor of Differentiation Protein 2, Mice, Mice, Inbred C57BL, Molecular Sequence Data, Nuclear Proteins, Repressor Proteins, Stem Cells, Transcription Factors
Show Abstract · Added December 8, 2014
Dendritic cells (DCs) comprise two major subsets, the interferon (IFN)-producing plasmacytoid DCs (pDCs) and antigen-presenting classical DCs (cDCs). The development of pDCs is promoted by E protein transcription factor E2-2, whereas E protein antagonist Id2 is specifically absent from pDCs. Conversely, Id2 is prominently expressed in cDCs and promotes CD8(+) cDC development. The mechanisms that control the balance between E and Id proteins during DC subset specification remain unknown. We found that the loss of Mtg16, a transcriptional cofactor of the ETO protein family, profoundly impaired pDC development and pDC-dependent IFN response. The residual Mtg16-deficient pDCs showed aberrant phenotype, including the expression of myeloid marker CD11b. Conversely, the development of cDC progenitors (pre-DCs) and of CD8(+) cDCs was enhanced. Genome-wide expression and DNA-binding analysis identified Id2 as a direct target of Mtg16. Mtg16-deficient cDC progenitors and pDCs showed aberrant induction of Id2, and the deletion of Id2 facilitated the impaired development of Mtg16-deficient pDCs. Thus, Mtg16 promotes pDC differentiation and restricts cDC development in part by repressing Id2, revealing a cell-intrinsic mechanism that controls subset balance during DC development.
© 2014 Ghosh et al.
1 Communities
1 Members
0 Resources
18 MeSH Terms
Myeloid translocation gene 16 is required for maintenance of haematopoietic stem cell quiescence.
Fischer MA, Moreno-Miralles I, Hunt A, Chyla BJ, Hiebert SW
(2012) EMBO J 31: 1494-505
MeSH Terms: Animals, Basic Helix-Loop-Helix Transcription Factors, Binding Sites, Cells, Cultured, E2F2 Transcription Factor, Gene Expression, Hematopoietic Stem Cells, Leukemia, Myeloid, Acute, Mice, Mice, Inbred C57BL, Mice, Nude, Nuclear Proteins, S Phase, Transcription Factors
Show Abstract · Added November 26, 2013
The t(8;21) and t(16;21) that are associated with acute myeloid leukaemia disrupt two closely related genes termed Myeloid Translocation Genes 8 (MTG8) and 16 (MTG16), respectively. Many of the transcription factors that recruit Mtg16 regulate haematopoietic stem and progenitor cell functions and are required to maintain stem cell self-renewal potential. Accordingly, we found that Mtg16-null bone marrow (BM) failed in BM transplant assays. Moreover, when removed from the animal, Mtg16-deficient stem cells continued to show defects in stem cell self-renewal assays, suggesting a requirement for Mtg16 in this process. Gene expression analysis indicated that Mtg16 was required to suppress the expression of several key cell-cycle regulators including E2F2, and chromatin immunoprecipitation assays detected Mtg16 near an E2A binding site within the first intron of E2F2. BrdU incorporation assays indicated that in the absence of Mtg16 more long-term stem cells were in the S phase, even after competitive BM transplantation where normal stem and progenitor cells are present, suggesting that Mtg16 plays a role in the maintenance of stem cell quiescence.
2 Communities
1 Members
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14 MeSH Terms
Identification of a Drosophila Myb-E2F2/RBF transcriptional repressor complex.
Lewis PW, Beall EL, Fleischer TC, Georlette D, Link AJ, Botchan MR
(2004) Genes Dev 18: 2929-40
MeSH Terms: Animals, Chromatography, Gel, Drosophila, Drosophila Proteins, E2F2 Transcription Factor, Immunoprecipitation, Proto-Oncogene Proteins c-myb, Repressor Proteins, Retinoblastoma Protein, Transcription Factors
Show Abstract · Added February 20, 2015
The Drosophila Myb complex has roles in both activating and repressing developmentally regulated DNA replication. To further understand biochemically the functions of the Myb complex, we fractionated Drosophila embryo extracts relying upon affinity chromatography. We found that E2F2, DP, RBF1, RBF2, and the Drosophila homolog of LIN-52, a class B synthetic multivulva (synMuv) protein, copurify with the Myb complex components to form the Myb-MuvB complex. In addition, we found that the transcriptional repressor protein, lethal (3) malignant brain tumor protein, L(3)MBT, and the histone deacetylase, Rpd3, associated with the Myb-MuvB complex. Members of the Myb-MuvB complex were localized to promoters and were shown to corepress transcription of developmentally regulated genes. These and other data now link together the Myb and E2F2 complexes in higher-order assembly to specific chromosomal sites for the regulation of transcription.
0 Communities
1 Members
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10 MeSH Terms
E2F-1 and E2F-3 are functionally distinct in their ability to promote myeloid cell cycle progression and block granulocyte differentiation.
Strom DK, Cleveland JL, Chellappan S, Nip J, Hiebert SW
(1998) Cell Growth Differ 9: 59-69
MeSH Terms: Apoptosis, Carrier Proteins, Cell Cycle, Cell Cycle Proteins, Cell Differentiation, Cell Line, DNA-Binding Proteins, E2F Transcription Factors, E2F1 Transcription Factor, E2F2 Transcription Factor, E2F3 Transcription Factor, E2F4 Transcription Factor, E2F5 Transcription Factor, Gene Expression Regulation, Granulocyte Colony-Stimulating Factor, Granulocytes, Humans, Interleukin-3, Retinoblastoma-Binding Protein 1, Transcription Factor DP1, Transcription Factors, Tumor Cells, Cultured
Show Abstract · Added June 10, 2010
Interleukin 3 (IL-3)-dependent 32D.3 myeloid cells are an attractive model system for the analysis of hematopoietic cell growth, differentiation, and apoptosis. In these cells, E2F-3, E2F-4, and DP-1 are regulated by both IL-3 and granulocyte colony-stimulating factor (G-CSF), whereas E2F-1 was expressed at low levels and was not regulated by either cytokine. E2F-2 and E2F-5 were not detectable. To examine phenotypes associated with the loss of normal cell cycle regulation by pRb, we established E2F-1- and E2F-3-overexpressing cell lines. In contrast to E2F-1, E2F-3 overexpression did not accelerate apoptosis or promote S-phase entry in the absence of IL-3, demonstrating that they are not functionally redundant. In addition, when cells were cultured in G-CSF to stimulate granulocytic differentiation, E2F-1 overexpression overrode survival functions provided by G-CSF and serum and induced apoptosis. In contrast, cells overexpressing E2F-3 exhibited normal granulocytic differentiation. Bcl-2 coexpression blocked E2F-1-induced apoptosis in the presence of G-CSF. However, these cells were blocked in the granulocytic differentiation program at the metamyelocyte stage and remained dependent on G-CSF for continuous culture. Cells overexpressing both E2F-1 and Bcl-2 exhibited slowed but continuous cell cycling in the absence of IL-3 until they eventually succumbed to apoptosis. Therefore, E2F-1, but not E2F-3, can temporally replace the requirement for growth factors to promote cell cycle progression, and in terminally differentiating cells, this leads to a block in differentiation and induction of apoptosis.
1 Communities
1 Members
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22 MeSH Terms