Nuclear Factor I-C Regulates TGF-β-dependent Hair Follicle Cycling*

Plasari, Genta; Edelmann, Simone; Hogger, Florence; Dusserre, Yves; Mermod, Nicolas; Calabrese, Alessandra

doi:10.1074/jbc.m110.120659

Cited by 32 publications

(31 citation statements)

References 60 publications

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“…Our interpretation of a regulatory interplay between Nfix and cell cycle inhibitors, such as p21, is also supported by a previously described role of Nfix in the regulation of mitogenic pathways in other cell types (Nebl et al, 1994). Our conclusions are also in line with prior observations of regulatory relationships between TGF-b and other Nfi species (Plasari et al, 2009;Plasari et al, 2010) and of BMP7 and Matn2 (Ichikawa et al, 2008) to control the timing of skin-wound healing. In keeping with these findings, we observed severe wound-healing defects in Matn2 2/2 mice on a C57BL/6 genetic background (F. Deák and I.…”

Section: Research Articlesupporting

confidence: 92%

“…Nfi proteins have been implicated in the control of adult stem cells and tissue regeneration in connection with TGF-b signaling (Plasari et al, 2009;Plasari et al, 2010). Nfix has been shown to drive a transcriptional switch from embryonic to fetal myogenesis in vivo and in C2 culture by suppressing the effect of Nfia and activating fetal muscle genes (Messina et al, 2010).…”

Section: Matn2 Is Required For C2 Myoblast Differentiationmentioning

confidence: 99%

“…Accordingly, other members of the NFI family have been implicated in other regenerative processes of adult tissue in the context of TGF-b signaling. For instance, Nfic has been implicated in tooth morphogenesis, skin-wound healing and the onset of the follicle cycle leading to hair regeneration (Lee et al, 2009;Plasari et al, 2009;Plasari et al, 2010). An NFIC isoform was shown to harbor a TGF-b-responsive domain, and NFI-binding sites acting as TGF-b-responsive elements have been reported in several other ECM genes (Alevizopoulos et al, 1995;Alonso et al, 1996;Iozzo et al, 1997).…”

Section: Research Articlementioning

confidence: 99%

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Extracellular deposition of matrilin-2 controls the timing of the myogenic program during muscle regeneration

Deák¹,

Mátés²,

Korpos³

et al. 2014

Development

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BSTRACTHere, we identify a role for the matrilin-2 (Matn2) extracellular matrix protein in controlling the early stages of myogenic differentiation. We observed Matn2 deposition around proliferating, differentiating and fusing myoblasts in culture and during muscle regeneration in vivo. Silencing of Matn2 delayed the expression of the Cdk inhibitor p21 and of the myogenic genes Nfix, MyoD and Myog, explaining the retarded cell cycle exit and myoblast differentiation. Rescue of Matn2 expression restored differentiation and the expression of p21 and of the myogenic genes. TGF-b1 inhibited myogenic differentiation at least in part by repressing Matn2 expression, which inhibited the onset of a positive-feedback loop whereby Matn2 and Nfix activate the expression of one another and activate myoblast differentiation. In vivo, myoblast cell cycle arrest and muscle regeneration was delayed in Matn2 2/2 relative to wild-type mice. The expression levels of Trf3 and myogenic genes were robustly reduced in Matn2 2/2 fetal limbs and in differentiating primary myoblast cultures, establishing Matn2 as a key modulator of the regulatory cascade that initiates terminal myogenic differentiation. Our data thus identify Matn2 as a crucial component of a genetic switch that modulates the onset of tissue repair.

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Section: Research Articlesupporting

confidence: 92%

Section: Matn2 Is Required For C2 Myoblast Differentiationmentioning

confidence: 99%

Section: Research Articlementioning

confidence: 99%

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Extracellular deposition of matrilin-2 controls the timing of the myogenic program during muscle regeneration

Deák¹,

Mátés²,

Korpos³

et al. 2014

Development

Self Cite

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“…TGF-β represses the expression human adenine nucleotide translocator-2 (ANT2) and this repression is NF1-dependent [49,50]. Another set of data identify the growing importance of NF1 in TGF-β signaling during skin wound healing and hair follicule cycling [51,52]. During in vitro odontoblast differentiation, NF1-C expression level is inversely proportional to the level of TGF-β signaling molecules.…”

Section: Nf1 Protein In Signaling Pathwaysmentioning

confidence: 99%

New insights into the role of NF1 in cancer

Sabová

Kretova²,

Luciaková³

2013

neo

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NF1 proteins are a family of transcription factors that act either as repressors or as activators. Functional studies indicate that NF1 participate in signaling pathways that regulate cell viability, proliferation and differentiation. Participation in regulation of genes important for tumor progression and metastasizing suggests a potential value of NF1 as a prognostic factor for certain types of cancer.

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“…These postnatal tooth defects appear to be mediated at least in part by antagonistic interactions between NFIC and the TGF-b signaling pathway during tooth development (Lee et al, 2011). In addition, NFIC interacts with TGF-b signaling during postnatal wound healing (Plasari et al, 2010) suggesting that NFIC-TGF-b interactions may represent a recurrent theme in postnatal NFIC function. More recently, NFIC has been shown to play a major role in postnatal osteoblast maturation through the regulation of the key osteoblast transcription factor Osterix .…”

Section: Nfis Are Potential Drivers Of Medulloblastoma Tumorigenesismentioning

confidence: 99%

The function of NFIX during developmental and adult neurogenesis

Harris¹

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Understanding the transcription factor proteins that control the biology of neural stem cells during embryogenesis provides insight into brain development as well as neurodevelopmental disorders.Likewise, studying the function of transcription factors in adult neural stem cells allows us to appreciate the dynamics of these cells and their contribution to normal cognitive function. It also provides a knowledge base so as to one day harness the activity of adult neural stem cells to treat degenerative conditions of the nervous system.One family of transcription factors key to brain development are the Nuclear Factor Ones (NFIs).Comprised of four members in mammals (NFIA, NFIB, NFIC and NFIX) these proteins promote both neuronal and glial differentiation during mouse forebrain development, and in general, appear to have a highly similar function. This thesis addressed two outstanding questions regarding the function of one these proteins, NFIX, in mouse neural stem cell biology. The first question concerned refining our understanding of NFIX function during forebrain development by determining, which stage of neuron differentiation, from a stem cell to a mature neuron, is The second question I addressed in this thesis, was that if NFI proteins are so important for regulating neural stem cell biology during brain development, then do they also regulate adult neural stem cell biology? I addressed this question by breeding inducible, conditional mice to allow for deletion of Nfix from adult hippocampal neural stem cells and separately, immature neurons. I found that NFIX is essential for adult-borne neuron differentiation, so that in the absence of NFIX, mature neurons are not generated and behavioural deficits ensue. Mechanistically, we found that NFIX is essential for primary dendrite formation, and that without NFIX a proportion of adult hippocampal progenitors switch fate to become oligodendrocytes or aberrantly express increased levels of oligodendrocyte mRNA. In addition to demonstrating the absolute requirement of the NFIX protein for the generation of adult-borne neurons, these findings reveal the surprising tri-

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Nuclear Factor I-C Regulates TGF-β-dependent Hair Follicle Cycling*

Cited by 32 publications

References 60 publications

Extracellular deposition of matrilin-2 controls the timing of the myogenic program during muscle regeneration

Extracellular deposition of matrilin-2 controls the timing of the myogenic program during muscle regeneration

New insights into the role of NF1 in cancer

The function of NFIX during developmental and adult neurogenesis

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