Antagonistic activities of Rho and Rac GTPases underlie the transition from neural crest delamination to migration

Shoval, Irit; Kalcheim, Chaya

doi:10.1002/dvdy.23799

Cited by 50 publications

(41 citation statements)

References 62 publications

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“…Numerous studies have shown that neural crest derivatives are formed in a ventral-to-dorsal sequence (Baker et al, 1997; Krispin et al, 2010; Lumsden et al, 1991; McKinney et al, 2013; Nitzan et al, 2013; Osumi-Yamashita et al, 1994; Shoval and Kalcheim, 2012). It is interesting to note that, in the study by Lumsden et al (Lumsden et al, 1991), although no attempt was made to label distinct regions of the neural fold, the authors found that, when the neural fold in the midbrain was labeled at early stages, only labeling of the ectomesenchyme was observed in the majority of cases.…”

Section: Discussionmentioning

confidence: 99%

“…Developmental heterogeneity exists within neural crest-derived populations, at least when they first emerge from the neural epithelium in vitro (Henion and Weston, 1997) and in vivo (Krispin et al, 2010; McKinney et al, 2013; Nitzan et al, 2013; Shoval and Kalcheim, 2012). Moreover, a population of mesenchyme cells precociously emerges from lateral cranial neural fold epithelium and enters the branchial arches before other cells emerge from the neural tube (Hill and Watson, 1958; Nichols, 1981).…”

Section: Introductionmentioning

confidence: 99%

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Cell delamination in the mesencephalic neural fold and its implication for the origin of ectomesenchyme

Lee

Nagai²,

Nakaya³

et al. 2013

Development

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The neural crest is a transient structure unique to vertebrate embryos that gives rise to multiple lineages along the rostrocaudal axis. In cranial regions, neural crest cells are thought to differentiate into chondrocytes, osteocytes, pericytes and stromal cells, which are collectively termed ectomesenchyme derivatives, as well as pigment and neuronal derivatives. There is still no consensus as to whether the neural crest can be classified as a homogenous multipotent population of cells. This unresolved controversy has important implications for the formation of ectomesenchyme and for confirmation of whether the neural fold is compartmentalized into distinct domains, each with a different repertoire of derivatives. Here we report in mouse and chicken that cells in the neural fold delaminate over an extended period from different regions of the cranial neural fold to give rise to cells with distinct fates. Importantly, cells that give rise to ectomesenchyme undergo epithelial-mesenchymal transition from a lateral neural fold domain that does not express definitive neural markers, such as Sox1 and N-cadherin. Additionally, the inference that cells originating from the cranial neural ectoderm have a common origin and cell fate with trunk neural crest cells prompted us to revisit the issue of what defines the neural crest and the origin of the ectomesenchyme.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cell delamination in the mesencephalic neural fold and its implication for the origin of ectomesenchyme

Lee

Nagai²,

Nakaya³

et al. 2013

Development

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“…These signals are capable of activating numerous intracellular pathways; however, convergent regulation of common downstream components, such as Rho and Rac, serves as a key integration point (Berndt, Clay, Langenberg, & Halloran, 2008; Clay & Halloran, 2014; Liu & Jessell, 1998; Shoval & Kalcheim, 2012; Theveneau & Mayor, 2012). Newly developed high-resolution imaging techniques and genetic tools will continue to provide unique insight into how entire populations of cells are guided into distinct migratory routes and destinations during embryogenesis (Clay & Halloran, 2010).…”

Section: Molecular Regulators Of Neural Crest Migrationmentioning

confidence: 99%

Molecular Control of the Neural Crest and Peripheral Nervous System Development

Newbern

2015

Current Topics in Developmental Biology

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A transient and unique population of multipotent stem cells, known as neural crest cells (NCCs), generate a bewildering array of cell types during vertebrate development. An attractive model among developmental biologists, the study of NCC biology has provided a wealth of knowledge regarding the cellular and molecular mechanisms important for embryogenesis. Studies in numerous species have defined how distinct phases of NCC specification, proliferation, migration, and survival contribute to the formation of multiple functionally distinct organ systems. NCC contributions to the peripheral nervous system (PNS) are well known. Critical developmental processes have been defined that provide outstanding models for understanding how extracellular stimuli, cell–cell interactions, and transcriptional networks cooperate to direct cellular diversification and PNS morphogenesis. Dissecting the complex extracellular and intracellular mechanisms that mediate the formation of the PNS from NCCs may have important therapeutic implications for neurocristopathies, neuropathies, and certain forms of cancer.

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“…In addition, RhoV and RhoU, which do not signal through ROCK, are expressed in Xenopus and chick NCCs, and have functions in NCC induction and migration (Fort et al, 2011;Guémar et al, 2007;Notarnicola et al, 2008). In addition, Rac1 promotes chick NCC migration and Rac activation is influenced by Rho (Shoval and Kalcheim, 2012). It will be important to determine how Rho family members function together in NCC EMT and to further uncover the diverse molecular processes that may be used by NCCs in different species and populations to ultimately carry out EMT.…”

Section: Research Articlementioning

confidence: 99%

Rho activation is apically restricted by Arhgap1 in neural crest cells and drives epithelial-to-mesenchymal transition

Clay

Halloran

2013

Development

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Epithelial-to-mesenchymal transitions (EMTs) are crucial for morphogenesis and carcinoma metastasis, yet mechanisms controlling the underlying cell behaviors are poorly understood. RhoGTPase signaling has been implicated in EMT; however, previous studies have yielded conflicting results regarding Rho function, and its role in EMT remains poorly understood. Elucidation of precise Rho functions has been challenging because Rho signaling is highly context dependent and its activity is tightly regulated spatiotemporally within the cell. To date, few studies have examined how Rho affects cell motility in intact organisms, and the pattern of Rho activity during motile cell behaviors of EMT has not been determined in any system. Here, we image endogenous active Rho during EMT in vivo, and analyze effects of Rho and Rho-kinase (ROCK) manipulation on cell motility in vivo. We show that Rho is activated in a discrete apical region of premigratory neural crest cells during EMT, and Rho-ROCK signaling is essential for apical detachment and generation of motility within the neuroepithelium, a process that has been poorly understood. Furthermore, we find that Arhgap1 restricts Rho activation to apical areas, and this restriction is necessary for detachment. Our results provide new insight into mechanisms controlling local Rho activation and how it affects dynamic cell behaviors and actomyosin contraction during key steps of EMT in an intact living organism.

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Antagonistic activities of Rho and Rac GTPases underlie the transition from neural crest delamination to migration

Cited by 50 publications

References 62 publications

Cell delamination in the mesencephalic neural fold and its implication for the origin of ectomesenchyme

Cell delamination in the mesencephalic neural fold and its implication for the origin of ectomesenchyme

Molecular Control of the Neural Crest and Peripheral Nervous System Development

Rho activation is apically restricted by Arhgap1 in neural crest cells and drives epithelial-to-mesenchymal transition

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