Stage-Specific Control of Neural Crest Stem Cell Proliferation by the Small Rho GTPases Cdc42 and Rac1

Fuchs, Sebastian; Herzog, Dominik; Sumara, Grzegorz; Büchmann-Møller, Stine; Civenni, Gianluca; Wu, Xunwei; Chrostek-Grashoff, Anna; Suter, Ueli; Ricci, Roméo; Relvas, João B.; Brakebusch, Cord; Sommer, Lukas

doi:10.1016/j.stem.2009.01.017

Cited by 96 publications

(90 citation statements)

References 47 publications

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“…However, once NCC have reached their target site, Rac1 and Cdc42 deletion increases their proliferation rate. 23 On the other hand, Rac1 may provide anti-apoptotic signal. Pro-apoptotic signal induced by Ras overexpression is overridden by a dominant negative form of Rac1.…”

Section: Down-regulation Of Rho Gtpases and Tumorigenesismentioning

confidence: 99%

Inhibition of Cdc42 and Rac1 activities in pheochromocytoma, the adrenal medulla tumor

et al. 2016

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Altered Rho GTPase signaling has been linked to many types of cancer. As many small G proteins, Rho GTPases cycle between an active and inactive state thanks to specific regulators that catalyze exchange of GDP into GTP (Rho-GEF) or hydrolysis of GTP into GDP (Rho-GAP). Recent studies have shown that alteration takes place either at the level of Rho proteins themselves (expression levels, point mutations) or at the level of their regulators, mostly RhoGEFs and RhoGAPs. Most reports describe Rho GTPases gain of function that may participate to the tumorigenesis processes. In contrast, we have recently reported that decreased activities of Cdc42 and Rac1 as well as decreased expression of 2 Rho-GEFs, FARP1 and ARHGEF1, correlate with pheochromocytomas, a tumor developing in the medulla of the adrenal gland (Croise et al., Endocrine Related Cancer, 2016). Here we highlight the major evidence and further study the correlation between Rho GTPases activities and expression levels of ARHGEF1 and FARP1. Finally we also discuss how the decrease of Cdc42 and Rac1 activities may help human pheochromocytomas to develop and comment the possible relationship between FARP1, ARHGEF1 and the 2 Rho GTPases Cdc42 and Rac1 in tumorigenesis.

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Section: Down-regulation Of Rho Gtpases and Tumorigenesismentioning

confidence: 99%

Inhibition of Cdc42 and Rac1 activities in pheochromocytoma, the adrenal medulla tumor

et al. 2016

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“…To determine the self-renewal potential of PAderived mesenchymal progenitor cells, single cells were cultured in sphere medium permissive for self-renewal of NCSCs [28]. PA cells possessed a limited sphere-forming potential and could only be passaged efficiently up to three passages (Supporting Information Fig.…”

Section: Identification and Characterization Of Nc-derived Mesenchymamentioning

confidence: 99%

Transforming Growth Factor β-Mediated Sox10 Suppression Controls Mesenchymal Progenitor Generation in Neural Crest Stem Cells

et al. 2011

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During vertebrate development, neural crest stem cells (NCSCs) give rise to neural cells of the peripheral nervous system and to a variety of mesenchymal cell types, including smooth muscle, craniofacial chondrocytes, and osteocytes. Consistently, mesenchymal stem cells (MSCs) have recently been shown to derive in part from the neural crest (NC), although the mechanisms underlying MSC generation remains to be identified. Here, we show that transforming growth factor b (TGFb)-mediated suppression of the NCSC transcription factor Sox10 induces a switch in neural to mesenchymal potential in NCSCs. In vitro and in vivo, TGFb signal inactivation results in persistent Sox10 expression, decreased cell cycle exit, and perturbed generation of mesenchymal derivatives, which eventually leads to defective morphogenesis. In contrast, TGFb-mediated downregulation of Sox10 or its genetic inactivation suppresses neural potential, confers mesenchymal potential to NC cells in vitro, and promotes cell cycle exit and precocious mesenchymal differentiation in vivo. Thus, negative regulation of Sox10 by TGFb signaling promotes the generation of mesenchymal progenitors from NCSCs. Our study might lay the grounds for future applications demanding defined populations of MSCs for regenerative medicine. STEM CELLS 2011;29:689-699 Disclosure of potential conflicts of interest is found at the end of this article.

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“…The small Rho GTPases Cdc42 and Rac1 are essential for the proliferation control through the EGF pathway in late (7) but not early (6) NCSCs [30]. …”

Section: Rac1 and Cdc42mentioning

confidence: 99%

Stage- and area-specific control of stem cells in the developing nervous system

Falk¹,

Sommer²

2009

Current Opinion in Genetics & Development

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The spatiotemporal control of proliferation and differentiation in neural stem cells (NSCs) is essential to produce a functional nervous system (NS). Stem cells in different areas and at different time points during development have to produce different types of cells in a precise manner. Recent studies uncovered a plethora of cell extrinsic as well as intrinsic factors that play crucial roles in the area-specific and stage-specific control of NSCs. Moreover, recapitulation of the spatiotemporal specification of NSCs in vitro opens new avenues for future applications. In this review, we have selected some key molecules to discuss the mechanisms underlying the spatiotemporal regulation of NSC development. Stage-and Area-Specific Control of Stem Cells in the Developing Nervous SystemSven Falk 1 , Lukas Sommer Summary of recent advancesThe spatiotemporal control of proliferation and differentiation in neural stem cells ( In this review, we have selected some key molecules to discuss the mechanisms underlying the spatiotemporal regulation of NSC development.

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Stage-Specific Control of Neural Crest Stem Cell Proliferation by the Small Rho GTPases Cdc42 and Rac1

Cited by 96 publications

References 47 publications

Inhibition of Cdc42 and Rac1 activities in pheochromocytoma, the adrenal medulla tumor

Inhibition of Cdc42 and Rac1 activities in pheochromocytoma, the adrenal medulla tumor

Transforming Growth Factor β-Mediated Sox10 Suppression Controls Mesenchymal Progenitor Generation in Neural Crest Stem Cells

Stage- and area-specific control of stem cells in the developing nervous system

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