Collective Chemotaxis Requires Contact-Dependent Cell Polarity

Théveneau, Eric; Marchant, Lorena; Kuriyama, Sei; Gull, Mazhar; Moepps, Barbara; Parsons, Maddy; Mayor, Roberto

doi:10.1016/j.devcel.2010.06.012

Cited by 486 publications

(887 citation statements)

References 51 publications

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“…The pathway by which Rac1 inactivates RhoA is blocked and these lines have already been shown to have increased levels of RhoA [17]. Blocking N-cadherin on NC cells prevented homotypic CIL and groups of cells invaded each other and overlapped [10]. In NIH3T3 fibroblasts the increased Rac1 activity results in p190RhoGAP translocation to adherens junctions (AJs) where it associates with the cadherin complex via transient binding to p120-catenin [17].…”

Section: Discussionmentioning

confidence: 99%

The effects of modifying RhoA and Rac1 activities on heterotypic contact inhibition of locomotion

Anear

Parish

2012

FEBS Letters

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a b s t r a c tContact inhibition of locomotion (CIL) occurs when a cell ceases moving in the same direction following contact with another cell. Homotypic and heterotypic CIL occur between cells of the same and different types, respectively. Using Abercrombie's confronted explants assay we studied the effect of changing Rac1 or RhoA activities on heterotypic CIL between NIH3T3 and chicken heart fibroblasts. Both dominant active (L61) and dominant negative (N17) Rac1 expressed in NIH3T3 cells resulted in loss of heterotypic CIL. N17Rac1 expression caused RhoA activation. Increasing RhoA activity directly (V14RhoA) or indirectly (downregulation of N-cadherin or p120-catenin) also resulted in loss of CIL. High RhoA activity has been associated with tumour invasion and our results are consistent with loss of heterotypic CIL playing a role.

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Section: Discussionmentioning

confidence: 99%

The effects of modifying RhoA and Rac1 activities on heterotypic contact inhibition of locomotion

Anear

Parish

2012

FEBS Letters

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“…If Pax3/Zic1 drives NC specification, one would expect that these cells would display the molecular signature of cells undergoing an EMT. In particular, a cadherin switch occurs before EMT: e-cadherin is expressed in cohesive epithelial/neuroepithelial cells, whereas n-cadherin is expressed in migrating NC in quail, mouse, and frog (18,19). On Pax3 or Zic1 induction, e-cadherin Fig.…”

Section: Resultsmentioning

confidence: 99%

Pax3 and Zic1 drive induction and differentiation of multipotent, migratory, and functional neural crest inXenopusembryos

Milet

Maczkowiak

Roche

et al. 2013

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

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Defining which key factors control commitment of an embryonic lineage among a myriad of candidates is a longstanding challenge in developmental biology and an essential prerequisite for developing stem cell-based therapies. Commitment implies that the induced cells not only express early lineage markers but further undergo an autonomous differentiation into the lineage. The embryonic neural crest generates a highly diverse array of derivatives, including melanocytes, neurons, glia, cartilage, mesenchyme, and bone. A complex gene regulatory network has recently classified genes involved in the many steps of neural crest induction, specification, migration, and differentiation. However, which factor or combination of factors is sufficient to trigger full commitment of this multipotent lineage remains unknown. Here, we show that, in contrast to other potential combinations of candidate factors, coactivating transcription factors Pax3 and Zic1 not only initiate neural crest specification from various early embryonic lineages in Xenopus and chicken embryos but also trigger full neural crest determination. These two factors are sufficient to drive migration and differentiation of several neural crest derivatives in minimal culture conditions in vitro or ectopic locations in vivo. After transplantation, the induced cells migrate to and integrate into normal neural crest craniofacial target territories, indicating an efficient spatial recognition in vivo. Thus, Pax3 and Zic1 cooperate and execute a transcriptional switch sufficient to activate full multipotent neural crest development and differentiation.neural crest developmental program | ectoderm to neural crest transcriptional switch T he neural crest, a transient embryonic cell population, develops into an amazing array of derivatives, including peripheral nervous system, pigment cells, cartilage, mesenchyme, and bone (1). During neural development, definitive neural crest (NC) induction is preceded by formation of a neural border territory between the neural plate and the nonneural ectoderm. This region is initiated by transcription factor TFAP2-α (AP2a, transcription factor activating enhancer binding protein 2 alpha) and reinforced by Hairy2, Msx1, and AP2a itself along with secreted bone morphogenetic protein (BMP) antagonists. In addition, Pax3/Pax7, Gbx2, and Zic1 are also essential for neural border specification (2-8). In turn, these transcription factors cooperate to activate the NC specifiers snail2 (snai2), soxE (sox8, 9, 10), and foxd3 in the ectoderm (reviewed in ref. 9). Although each neural border specifier is necessary for NC formation in vivo, none of these factors alone is sufficient to initiate NC induction in the ectoderm (3,7,8). Addition of a secreted BMP antagonist, a Wnt signal, or another transcription factor is needed to activate early NC specifiers (reviewed in ref. 10). In particular, Pax3 and Zic1 can synergize and initiate expression of early NC markers in blastula ectoderm (3,5,(7)(8)(9)(10)(11). However, it remains unknown which of t...

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“…Cell-cell adhesions after NC delamination are maintained usually by type II classical cadherins (Kuriyama et al, 2014;Theveneau et al, 2010). …”

Section: Epidermal-to-mesenchymal Transition (Emt)-basic Conceptmentioning

confidence: 99%

“…The role of Snail2 in the EMT of chick trunk NC cells is linked with the transcriptional repression of N-cadherins by interaction with LIM domain only protein 4 (Lmo4) (Ferronha et al, 2013). On the contrary, in Xenopus N-cadherins are only slightly downregulated during delamination and migration of cranial NC cells and have been shown to be crucial for the response to chemoattractants (Barriga et al, 2013;Theveneau et al, 2010).…”

Section: Loss Of Epithelial Polarity and Modulation Of Cell Adhesionmentioning

confidence: 99%

Controlled levels of canonical Wnt signaling are required for neural crest migration

Maj

Künneke

Loresch

et al. 2016

Developmental Biology

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Collective Chemotaxis Requires Contact-Dependent Cell Polarity

Cited by 486 publications

References 51 publications

The effects of modifying RhoA and Rac1 activities on heterotypic contact inhibition of locomotion

The effects of modifying RhoA and Rac1 activities on heterotypic contact inhibition of locomotion

Pax3 and Zic1 drive induction and differentiation of multipotent, migratory, and functional neural crest inXenopusembryos

Controlled levels of canonical Wnt signaling are required for neural crest migration

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