NF-Y cooperates with USF1/2 to induce the hematopoietic expression of HOXB4

Zhu, Jiang; Giannola, Diane; Zhang, Yi; Rivera, Adam J.; Emerson, Stephen G.

doi:10.1182/blood-2003-01-0251

Cited by 72 publications

(76 citation statements)

References 31 publications

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“…The ChIP analysis of HOX4 paralog promoters was performed as described in ref. 7. The primers were as follows.…”

Section: Methodsmentioning

confidence: 99%

“…Nuclear extracts were prepared as described in ref. 7. Ten micrograms of lysate was loaded onto each lane of SDS͞12% PAGE for separation and then blotted to Immobilon-P transfer membranes (Millipore).…”

Section: Methodsmentioning

confidence: 99%

“…Recently, we demonstrated that the trimeric transcription factor NF-Y activates the HOXB4 promoter in cooperation with upstream͞ubiquitous stimulating factor 1 and 2 (USF1͞2) in normal and malignant hematopoietic cells (6,7). Studies from other laboratories suggested that NF-Y is also a potent inducer for numerous other genes whose function likely influences stem cell (SC) function, including HOXB7, JunB, p27, CDK1, MDR1, and TGF␤R-II (8)(9)(10)(11)(12)(13).…”

mentioning

confidence: 99%

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NF-Ya activates multiple hematopoietic stem cell (HSC) regulatory genes and promotes HSC self-renewal

Zhu

Zhang

Joe

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…The ChIP analysis of HOX4 paralog promoters was performed as described in ref. 7. The primers were as follows.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

NF-Ya activates multiple hematopoietic stem cell (HSC) regulatory genes and promotes HSC self-renewal

Zhu

Zhang

Joe

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…Among these TFBS, sites for Cdx-1, USF, E12, IUF-1, Pbx-1, and c-Jun were found to be significantly enriched (P Ͻ 8 ϫ 10 Ϫ3 ) in these conserved sequences as compared with TFBS predicted on random noncoding sequences in the human genome (see footnote to Table 5). Cdx-1 and USF are known regulators of Hox genes (25,26), and because our loci contain a large number of Hox genes, many of the binding sites identified for these factors might be functional. The TFBS predicted on the CNS constitute targets for assaying the potential functions of the associated CNS.…”

Section: Transcription Factor Binding Sites (Tfbs) Within Cnsmentioning

confidence: 99%

Highly conserved syntenic blocks at the vertebrate Hox loci and conserved regulatory elements within and outside Hox gene clusters

Lee

Koh²,

Tay³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Hox genes in vertebrates are clustered, and the organization of the clusters has been highly conserved during evolution. The conservation of Hox clusters has been attributed to enhancers located within and outside the Hox clusters that are essential for the coordinated ''temporal'' and ''spatial'' expression patterns of Hox genes in developing embryos. To identify evolutionarily conserved regulatory elements within and outside the Hox clusters, we obtained contiguous sequences for the conserved syntenic blocks from the seven Hox loci in fugu and carried out a systematic search for conserved noncoding sequences (CNS) in the human, mouse, and fugu Hox loci. Our analysis has uncovered unusually large conserved syntenic blocks at the HoxA and HoxD loci. conserved noncoding sequences ͉ conserved synteny ͉ fugu ͉ global control region H ox genes code for homeodomain-containing transcription factors that determine the anterior-posterior patterning of tissues along the body axis of animals. In vertebrates, Hox genes are organized into tight clusters containing up to 14 paralogs. A remarkable feature of these clusters is that the positions of genes in the cluster are colinear with their spatial and temporal expression pattern along the anterior-posterior axis of the embryo. Hox genes at the 3Ј end of the cluster (see Fig. 1) express in the anterior segments of the embryo and are turned on relatively early during development, whereas genes at the 5Ј end express in the posterior segments and at a later stage during development (1). More than two decades after the discovery of Hox clusters, the molecular mechanisms underlying this orchestrated expression pattern of Hox genes and the selective pressure that has maintained the clustering and colinear organization of vertebrate Hox genes still are not well understood.The colinear organization of Hox genes has been shown to be essential for the temporal progression of expression but not for the spatial expression patterns. Transgenic Hox genes inserted at ectopic locations in the genome retain spatial expression to a large extent but fail to recapitulate their temporal pattern of regulation (1). The mechanism of colinear expression of vertebrate Hox genes may require coordinated alterations in the higher-order chromatin structure from one end of the cluster to the other (2). Such a mechanism could require the clustering and colinear organization of Hox genes to be strictly maintained.Another factor that may have contributed to the clustering and colinearity of Hox genes is the existence of global enhancers that regulate several genes in a manner independent of their local enhancers but dependent on their location in the cluster. Global control regions (GCRs) have been identified on either side of the HoxD cluster. The 5Ј HoxD GCR, regulating the expression of Lnp, Evx2, and posterior HoxD genes in developing digits and the central nervous system, is located Ϸ240 kb upstream of HoxD13 in the intergenic region between Atp5g3 and Lnp (3). The 3Ј HoxD GCR mapped downstream of HoxD1...

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“…(a) The expression of HOXB4, a master gene of hematopoietic stem cells (HSC), is driven by two important NF-Y sites: one in the promoter, which synergizes with nearby upstream transcription factor (USFs), and one in the intronic enhancer, which overlaps and synergizes with YY1 [9,18,19]. Retroviral infections of NF-YAs in mouse HSCs increased substantially their capacity to repopulate the bone marrow of immunocompromized animals, by enhancing the expression of several HOX genes, as well as Notch and Wnt signaling [19].…”

Section: Introductionmentioning

confidence: 99%

The Short Isoform of NF‐YA Belongs to the Embryonic Stem Cell Transcription Factor Circuitry

et al. 2012

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Totipotency of embryonic stem cells (ESCs) is controlled at the transcriptional level by a handful of transcription factors (TFs) that promote stemness and prevent differentiation. One of the most enriched DNA elements in promoters and enhancers of genes specifically active in ESCs is the CCAAT box, which is recognized by NF-Y, a trimer with histone-like subunits-NF-YB/NF-YC-and the sequence-specific NF-YA. We show that the levels of the short NF-YA isoform-NF-YAs-is high in mouse ESCs (mESCs) and drops after differentiation; a dominant negative mutant affects expression of important stem cells genes, directly and indirectly. Protein transfections of TAT-NF-YAs stimulate growth and compensate for withdrawal of leukemia inhibitory factor (LIF) in cell cultures. Bioinformatic analysis identifies NF-Y sites as highly enriched in genomic loci of stem TFs in ESCs. Specifically, 30%-50% of NANOG peaks have NF-Y sites and indeed NF-Y-binding is required for NANOG association to DNA. These data indicate that NF-Y belongs to the restricted circle of TFs that govern mESCs, and, specifically, that NF-YAs is the active isoform in these cells.

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NF-Y cooperates with USF1/2 to induce the hematopoietic expression of HOXB4

Cited by 72 publications

References 31 publications

NF-Ya activates multiple hematopoietic stem cell (HSC) regulatory genes and promotes HSC self-renewal

NF-Ya activates multiple hematopoietic stem cell (HSC) regulatory genes and promotes HSC self-renewal

Highly conserved syntenic blocks at the vertebrate Hox loci and conserved regulatory elements within and outside Hox gene clusters

The Short Isoform of NF‐YA Belongs to the Embryonic Stem Cell Transcription Factor Circuitry

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