The interferon-inducible gene, Ifi204, is transcriptionally activated in response to M-CSF, and its expression favors macrophage differentiation in myeloid progenitor cells

Dauffy, Jérémy; Mouchiroud, Guy; Bourette, Roland P.

doi:10.1189/jlb.0205083

Cited by 34 publications

(42 citation statements)

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“…The p204 gene was isolated as a macrophage-colony-stimulating factor (M-CSF)-responsive gene by using a gene trap approach in the interleukin (IL)-3-dependent myeloid FD-Fms cell line. Moreover forced expression of p204 strongly repressed the IL-3 and M-CSF-dependent proliferation, whereas it promoted the M-CSF-induced macrophage differentiation of FD-Fms cells (Dauffy et al, 2006). p204 may also play an important role in lymphocytic differentiation based on the observation that p204 mRNA levels are higher in less mature double-positive (CD4 ϩ CD8 ϩ ) thymocytes than in single-positive (CD4 ϩ or CD8ϩ) thymocytes (Deftos et al, 2000).…”

confidence: 99%

“…This is due at least in part to the binding of p204 to the Id proteins, including Id1, Id2, and Id3, and overcoming the inhibition by the Id proteins of MyoD activity in skeletal muscle differentiation, and Gata4 and Nkx2.5 activity in cardiac myocyte formation (Liu et al, 2002;Ding et al, 2006b). A recent publication revealed the involvement of p204 also in macrophage differentiation (Dauffy et al, 2006). The p204 gene was isolated as a macrophage-colony-stimulating factor (M-CSF)-responsive gene by using a gene trap approach in the interleukin (IL)-3-dependent myeloid FD-Fms cell line.…”

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p204 Protein Overcomes the Inhibition of Core Binding Factor α-1–mediated Osteogenic Differentiation by Id Helix-Loop-Helix Proteins

Luan

Yang

et al. 2008

MBoC

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Id proteins play important roles in osteogenic differentiation; however, the molecular mechanism remains unknown. In this study, we established that inhibitor of differentiation (Id) proteins, including Id1, Id2, and Id3, associate with core binding factor ␣-1 (Cbfa1) to cause diminished transcription of the alkaline phosphatase (ALP) and osteocalcin (OCL) gene, leading to less ALP activity and osteocalcin (OCL) production. Id acts by inhibiting the sequence-specific binding of Cbfa1 to DNA and by decreasing the expression of Cbfa1 in cells undergoing osteogenic differentiation. p204, an interferon-inducible protein that interacts with both Cbfa1 and Id2, overcame the Id2-mediated inhibition of Cbfa1-induced ALP activity and OCL production. We show that 1) p204 disturbed the binding of Id2 to Cbfa1 and enabled Cbfa1 to bind to the promoters of its target genes and 2) that p204 promoted the translocation from nucleus to the cytoplasm and accelerated the degradation of Id2 by ubiquitin-proteasome pathway during osteogenesis. Nucleus export signal (NES) of p204 is required for the p204-enhanced cytoplasmic translocation and degradation of Id2, because a p204 mutant lacking NES lost these activities. Together, Cbfa1, p204, and Id proteins form a regulatory circuit and act in concert to regulate osteoblast differentiation. INTRODUCTIONThe differentiation of uncommitted mesenchymal cells to osteoblasts is a fundamental process in embryonic development and bone repair. The bone morphogenetic proteins (BMPs) are important regulators of this process (Heldin et al., 1997;Miyazono et al., 2000). They function by binding cell surface receptors; signaling by Smad proteins; and activating bone-specific genes, including core binding factor ␣-1 (Cbfa1) (Ducy, 2000;Miyazono et al., 2001;Attisano and Wrana, 2002). This process is positively or negatively regulated by a variety of coactivators and corepressors (Ducy et al., 2000;Miyazono et al., 2001;Attisano and Wrana, 2002). Cbfa1, also known as Runx2, PeBP2␣A, Osf2, or AML3, is a member of the runt family of transcription factors. It is an essential transcription factor of osteoblast and bone formation (Ducy, 2000). During skeletal development, Cbfa1 is observed first in early mesenchymal condensations, and it is then principally expressed in osteoblasts . Cbfa1 Ϫ/Ϫ mice exhibit a complete lack of ossification, and they die immediately after birth (Komori et al., 1997). Cbfa1 maintains osteoblastic function by regulating the expression of several bone-specific genes such as osteopontin and osteocalcin and by controlling bone extracellular matrix deposition (Ducy, 2000). Mutations in Cbfa1 are found in 65-80% of individuals with cleidocranial dysplasia (CCD) (Lee et al., 1997;Mundlos and Olsen, 1997;Zhou et al., 1999). The molecular mechanisms underlying the pathogenesis of CCD are not completely defined. Some mutations of Cbfa1 abolish its DNA binding activity (Lee et al., 1997;Zhou et al., 1999) and others disturb the association of Cbfa1 to its binding partners, including Sma...

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confidence: 99%

p204 Protein Overcomes the Inhibition of Core Binding Factor α-1–mediated Osteogenic Differentiation by Id Helix-Loop-Helix Proteins

Luan

Yang

et al. 2008

MBoC

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“…4A). These include DUSP5, a negative-feedback regulator of Erk1/2, which inhibits macrophage differentiation and favors granulocytic differentiation (Grasset et al 2010), interferon-inducible gene 204 (Ifi204), which suppresses proliferation and favors differentiation (Dauffy et al 2006), and the adaptor proteins suppressor of cytokine signaling 1 (Socs1) and SKAP55-related (SKAP55R). Socs1 associates with CSF-1R pTyr-697 and pTyr721 binding sites to inhibit proliferation by an unknown mechanism (Bourette et al 2001).…”

Section: Er Stanley and V Chitumentioning

confidence: 99%

CSF-1 Receptor Signaling in Myeloid Cells

Stanley

Chiţu

2014

Cold Spring Harbor Perspectives in Biology

637

521

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The CSF-1 receptor (CSF-1R) is activated by the homodimeric growth factors colony-stimulating factor-1 (CSF-1) and interleukin-34 (IL-34). It plays important roles in development and in innate immunity by regulating the development of most tissue macrophages and osteoclasts, of Langerhans cells of the skin, of Paneth cells of the small intestine, and of brain microglia. It also regulates the differentiation of neural progenitor cells and controls functions of oocytes and trophoblastic cells in the female reproductive tract. Owing to this broad tissue expression pattern, it plays a central role in neoplastic, inflammatory, and neurological diseases. In this review we summarize the evolution, structure, and regulation of expression of the CSF-1R gene. We discuss the structures of CSF-1, IL-34, and the CSF-1R and the mechanism of ligand binding to and activation of the receptor. We further describe the pathways regulating macrophage survival, proliferation, differentiation, and chemotaxis downstream from the CSF-1R.

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“…12,14,15,[19][20][21][22][23][24] The current study sought to elucidate the role of p204 in chondrogenesis, with the special focus on chondrocyte hypertrophy, and the molecular events underlying this process. p204 demonstrated prominent expression in the growth plate prehypertrophic and hypertrophic chondrocytes ( Figure 1) and was found to be induced in the course of chondrocyte differentiation in vitro (Figure 2).…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, forced expression of p204 strongly repressed the IL-3-and M-CSF-dependent proliferation, whereas it promoted the M-CSF-induced macrophage differentiation of FD-Fms cells. 23 We previously reported that p204 acted as a transcriptional coactivator of Cbfa1 and therefore enhanced osteoblast differentiation 12 and that pRb is an essential linker between p204 and Cbfa1 thereby increasing its activity; 24 p204, pRb, Cbfa1 and Ids form a protein interaction network and act in concert in regulating the differentiation of pluripotent C2C12 to osteoblasts. 25 In this study, we describe the expression and function of p204 in hypertrophic chondrocyte differentiation as well as the molecular mechanism involved.…”

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Cbfa1-dependent expression of an interferon-inducible p204 protein is required for chondrocyte differentiation

Zhang

Kong

et al. 2008

Cell Death Differ

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We reported earlier that an interferon-inducible p204 protein serves as a cofactor of Cbfa1 and promotes osteogenesis. Here we establish that p204 demonstrates prominent expression in growth plate chondrocytes. It is differentially expressed in the course of bone morphogenetic protein-2-triggered chondrocyte differentiation of pluripotent C3H10T1/2 cells. This expression is probably due to the activation of p204 gene by Cbfa1 and repression by Sox5 transcription factor. Cbfa1 and Sox5 bind to the 5 0 -flanking regulatory region of p204 gene at their consensus binding elements. Overexpression of p204 accelerates chondrocyte hypertrophy, as revealed by enhanced expression of type X Collagen and matrix metalloproteinase-13; however, knockdown of p204 via an siRNA approach abolishes hypertrophic chondrocyte differentiation. p204 acts as a cofactor of Cbfa1 in chondrocyte hypertrophy: (1) overexpression of p204 augments, whereas suppression of p204 decreases, the Cbfa1-dependent transactivation of a Collagen X-specific reporter gene; (2) p204 enhances Cbfa1-mediated chondrocyte hypertrophy; and (3) p204 associates with Cbfa1 in chondrocyte differentiation. In addition, altered expression of p204 in chondrocyte hypertrophy was accompanied by altered levels of Indian hedgehog (IHH) and parathyroid hormone/parathyroid hormone-related peptide receptor-1 (PTHR1). Collectively, p204 is a novel regulator of chondrocyte differentiation by (1) acting as a coactivator of Cbfa1 and (2) affecting IHH/PTPrP signaling.

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The interferon-inducible gene, Ifi204, is transcriptionally activated in response to M-CSF, and its expression favors macrophage differentiation in myeloid progenitor cells

Cited by 34 publications

References 50 publications

p204 Protein Overcomes the Inhibition of Core Binding Factor α-1–mediated Osteogenic Differentiation by Id Helix-Loop-Helix Proteins

p204 Protein Overcomes the Inhibition of Core Binding Factor α-1–mediated Osteogenic Differentiation by Id Helix-Loop-Helix Proteins

CSF-1 Receptor Signaling in Myeloid Cells

Cbfa1-dependent expression of an interferon-inducible p204 protein is required for chondrocyte differentiation

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