GOOSECOID inhibits erythrocyte differentiation by competing with Rb for PU.1 binding in murine cells

Konishi, Yuko; Tominaga, Mari; Watanabe, Yuji; Imamura, Fumiya; Goldfarb, AN; Maki, Richard A.; Blum, Martin; Robertis, E. M. De; Tominaga, Akira

doi:10.1038/sj.onc.1203118

Cited by 20 publications

(24 citation statements)

References 42 publications

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“…Contrary to this, PU.1, a hematopoietic-specific transcription factor has been reported to interact GATA-1 showing functional antagonism in erythroid cells: ectopic expression of PU.1 in Xenopus embryos is sufficient to block erythropoiesis during normal development (Rekhtman et al, 1999). Misexpression of the dorsal mesodermal patterning factor goosecoid on the ventral side of Xenopus embryos results in inhibition of blood formation in early embryognesis, suggesting that goosecoid protein may interact with PU.1 (Konishi et al, 1999). The Ikaros family of zinc-finger transcription factors also plays an essential role as a master switch in hematopoiesis (Hansen et al, 1997;Durand et al, 1999).…”

Section: Perspectivesmentioning

confidence: 88%

Mechanisms of Egg Activation and Polyspermy Block in Amphibians and Comparative Aspects with Fertilization in Other Vertebrates

Iwao¹

2000

Zoological Science

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Section: Perspectivesmentioning

confidence: 88%

Mechanisms of Egg Activation and Polyspermy Block in Amphibians and Comparative Aspects with Fertilization in Other Vertebrates

Iwao¹

2000

Zoological Science

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“…PU.1 functions in concert with other transcription factors and cofactors, including c-Myb, C/EBPa (Oelgeschlager et al, 1996), NF-IL-6 (C/EBPd) (Nagulapalli et al, 1995), NF-EM-5/Pip (Eisenbeis et al, 1995), cFos (Bassuk and Leiden, 1995), c-Jun (Pongubala and Atchison, 1997), Rb (Konishi et al, 1999) and RUNX1/ AML1 (Zhang et al, 1994). We have previously reported that PU.1 interacts with CRE-binding protein (CBP) or p300, which functions as a coactivator for several transcription factors .…”

Section: Introductionmentioning

confidence: 99%

Site-specific DNA methylation by a complex of PU.1 and Dnmt3a/b

et al. 2005

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The Ets transcription factor PU.1 is a hematopoietic master regulator essential for the development of myeloid and B-cell lineages. As we previously reported, PU.1 sometimes represses transcription on forming a complex with mSin3A-histone deacetyl transferase-MeCP2. Here, we show an interaction between PU.1 and DNA methyltransferases, DNA methyltransferase (Dnmt)3a and Dnmt3b (Dnmt3s). Glutathione-S-transferase pulldown assay revealed that PU.1 directly interacted with the ATRX domain of Dnmt3s through the ETS domain. Dnmt3s repressed the transcriptional activity of PU.1 on a reporter construct with trimerized PU.1-binding sites. The repression was recovered by addition of 5-aza-deoxycitidine, a DNA methyltransferase inhibitor, but not trichostatin A, a histone deacetylase inhibitor. Bisulfite sequence analysis revealed that several CpG sites in the promoter region neighboring the PU.1-binding sites were methylated when Dnmt3s were coexpressed with PU.1. We also showed that the CpG sites in the p16 INK4A promoter were methylated by overexpression of PU.1 in NIH3T3 cells, accompanied by a downregulation of p16 INK4A gene expression. These results suggest that PU.1 may downregulate its target genes through an epigenetic modification such as DNA methylation.

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“…Recently, it has been demonstrated that GOOSECOID protein (GSC), a homoebox gene product, interacts with PU.1 via its N-terminal portion, which is also the binding site of Rb. Thus, GSC competitively inhibits the binding of Rb to PU.1, resulting in the suppression of blood formation in early embryogenesis (Konishi et al, 1999).…”

Section: Ets/rbmentioning

confidence: 99%