Physical and functional interactions between the transcription factor PU.1 and the coactivator CBP

Yamamoto, Hiroaki; Kihara-Negishi, Fumiko; Yamada, Toshiyuki; Hashimoto, Yuichi; Oikawa, Tsuneyuki

doi:10.1038/sj.onc.1202427

Cited by 109 publications

(82 citation statements)

References 50 publications

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“…We next wanted to investigate why histone acetylation levels were low in PU.1 Ϫ/Ϫ cells and in PUER cells at early time points of OHT induction. This was not due to the absence of nucleosomes, as shown by a ChIP (23,37), and work from our lab demonstrated that active c-fms regulatory elements recruit CBP (9). It has been shown previously that the activity of CBP can be regulated as well (35); it was therefore possible that CBP was recruited but was inactive.…”

Section: Resultsmentioning

confidence: 81%

A Two-Step, PU.1-Dependent Mechanism for Developmentally Regulated Chromatin Remodeling and Transcription of the c-fms Gene

Krysinska

Hoogenkamp

Ingram

et al. 2007

Molecular and Cellular Biology

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Hematopoietic stem cells and multipotent progenitors exhibit low-level transcription and partial chromatin reorganization of myeloid cell-specific genes including the c-fms (csf1R) locus. Expression of the c-fms gene is dependent on the Ets family transcription factor PU.1 and is upregulated during myeloid differentiation, enabling committed macrophage precursors to respond to colony-stimulating factor 1. To analyze molecular mechanisms underlying the transcriptional priming and developmental upregulation of the c-fms gene, we have utilized myeloid progenitors lacking the transcription factor PU.1. PU.1 can bind to sites in both the c-fms promoter and the c-fms intronic regulatory element (FIRE enhancer). Unlike wild-type progenitors, the PU.1 ؊/؊ cells are unable to express c-fms or initiate macrophage differentiation. When PU.1 was reexpressed in mutant progenitors, the chromatin structure of the c-fms promoter was rapidly reorganized. In contrast, assembly of transcription factors at FIRE, acquisition of active histone marks, and high levels of c-fms transcription occurred with significantly slower kinetics. We demonstrate that the reason for this differential activation was that PU.1 was required to promote induction and binding of a secondary transcription factor, Egr-2, which is important for FIRE enhancer activity. These data suggest that the c-fms promoter is maintained in a primed state by PU.1 in progenitor cells and that at FIRE PU.1 functions with another transcription factor to direct full activation of the c-fms locus in differentiated myeloid cells. The two-step mechanism of developmental gene activation that we describe here may be utilized to regulate gene activity in a variety of developmental pathways.

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Section: Resultsmentioning

confidence: 81%

A Two-Step, PU.1-Dependent Mechanism for Developmentally Regulated Chromatin Remodeling and Transcription of the c-fms Gene

Krysinska

Hoogenkamp

Ingram

et al. 2007

Molecular and Cellular Biology

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“…We ®rst analysed the e ects of the deletion mutants D1 ± 70, D74 ± 122 and D1 ± 100, on c-myc promoter activity. The N-terminal aa 1 ± 70 of PU.1 have been shown to encode the N-terminal TBP/RB binding domain (Hagemeier et al, 1993), and 1 ± 122 the transactivation and CBP binding domain (Fisher et al, 1998;Yamamoto et al, 1999). All these deletion mutants reduced c-myc promoter activity like the wild type PU.1 (Figure 5b).…”

Section: Pu1-mediated Repression Is Not Due To Sequestration Of Tranmentioning

confidence: 98%

In vivo complex formation of PU.1 with HDAC1 associated with PU.1-mediated transcriptional repression

et al. 2001

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“…The transcriptional activity of Spi-1 depends on its combinatorial association within multiprotein complexes. Some of these proteins are ubiquitous factors such as the basal transcription factor TFIID (Hagemeier et al, 1993) and the co-activator/integrator CBP (Yamamoto et al, 1999). Other Spi-1-interacting partners are tissue-specific as the B lymphoid factor NF-EM5/Pip (Perkel and Atchison, 1998;Brass et al, 1999), the myeloid regulators c-JUN , AML1 and C/EBPa (Petrovick et al, 1998) and the erythroid transcription factor GATA-1 (Rekhtman et al, 1999;Zhang et al, 1999;Zhang et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Multiple functional domains of the oncoproteins Spi-1/PU.1 and TLS are involved in their opposite splicing effects in erythroleukemic cells

et al. 2004

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The hematopoietic transcription factor Spi-1/PU.1 is an oncoprotein participating to the malignant transformation of proerythroblasts in the Friend erythroleukemia or in the erythroleukemic process developed in spi-1 transgenic mice. Overexpression of Spi-1 in proerythroblasts blocks their differentiation. We have shown that Spi-1 promotes the use of the proximal 5 0 -splice site during the E1A premRNA splicing and interferes with the effect of TLS (Translocated in LipoSarcoma) in this splicing assay. TLS was identified from chromosomal translocations in human liposarcoma and acute myeloid leukemia. Here, we determine the function of Spi-1 domains in splicing and in the interference with TLS. In transient transfection assays in erythroid cells, we show that the DNA binding domain cooperates with the transactivation domain or the PEST region of Spi-1 to modify the function of TLS in splicing. Interestingly, the 27 C-terminal amino acids, which determine the DNA binding activity of Spi-1, are necessary for the splicing function of Spi-1 as well as for its ability to interfere with TLS. Finally, we demonstrate that in leukemic proerythroblasts overexpressing Spi-1, TLS has lost its splicing effect. Thus, we hypothesize that oncogenic pathways in proerythroblasts may involve the ability of Spi-1 to alter splicing.

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Physical and functional interactions between the transcription factor PU.1 and the coactivator CBP

Cited by 109 publications

References 50 publications

A Two-Step, PU.1-Dependent Mechanism for Developmentally Regulated Chromatin Remodeling and Transcription of the c-fms Gene

A Two-Step, PU.1-Dependent Mechanism for Developmentally Regulated Chromatin Remodeling and Transcription of the c-fms Gene

In vivo complex formation of PU.1 with HDAC1 associated with PU.1-mediated transcriptional repression

Multiple functional domains of the oncoproteins Spi-1/PU.1 and TLS are involved in their opposite splicing effects in erythroleukemic cells

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