Early requirement of the transcriptional activator Sox9 for neural crest specification in Xenopus

Lee, Young Ho; Aoki, Yoshihiko; Hong, Chia Swee; Saint-Germain, Natasha; Credidio, Christine; Saint-Jeannet, Jean Pierre

doi:10.1016/j.ydbio.2004.07.036

Cited by 46 publications

(35 citation statements)

References 46 publications

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“…A second set of genes, termed ''late neural crest specifiers,'' is activated later in the forming neural crest in the dorsal neural tube. The temporal and spatial expression pattern of these regulators, like FoxD3 and SoxE, resembles those in other vertebrates (Aoki et al, 2003;Cheung et al, 2005;Dottori et al, 2001;Honore et al, 2003;Lee et al, 2004;Montero-Balaguer et al, 2006;Sasai et al, 2001;Sauka-Spengler et al, 2007;Spokony et al, 2002;Taylor and Labonne, 2005;Yan et al, 2005). Thus, this differs from earlier formulations of the NC-GRN in which there was a single category of neural crest specifier genes, with no discrimination in timing of early versus late phases.…”

Section: Agnathansmentioning

confidence: 79%

Evolution of the neural crest viewed from a gene regulatory perspective

Sauka‐Spengler

Bronner‐Fraser

2008

Genesis

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Summary: Neural crest cells are a vertebrate innovation and form a wide variety of embryonic cell types as diverse as peripheral neurons and facial skeleton. They undergo complex migration and differentiation processes from their site of origin in the developing central nervous system to their final destinations in the periphery. In this review, we summarize recent data on the current formulation of a gene regulatory network underlying neural crest formation and its roots at the base of the vertebrate lineage. Analyzing neural crest formation from a gene regulatory viewpoint provides insights into both the developmental mechanisms and evolutionary origins of this vertebrate-specific cell type. genesis 46:673-682,

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Section: Agnathansmentioning

confidence: 79%

Evolution of the neural crest viewed from a gene regulatory perspective

Sauka‐Spengler

Bronner‐Fraser

2008

Genesis

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“…Upregulation of neuron-specific transcription factors such as neurogenin1 (neurog1) and neurog2 are some of the first events in DRG neurogenesis (Greenwood et al, 1999;Ma et al, 1999;Perez et al, 1999;McGraw et al, 2008). Mechanisms that drive only some cells to activate these transcription programs while others assume glial fates instead are not well understood, although lateral inhibition via Notch/Delta signal (Hu et al, 2011;Mead and Yutzey, 2012), Hedgehog signaling (Ungos et al, 2003) and Wnt signaling (Lee et al, 2004) have been implicated.…”

Section: Introductionmentioning

confidence: 99%

Modulation of dorsal root ganglion development by ErbB signaling and the scaffold protein Sorbs3

et al. 2013

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The multipotent cells of the vertebrate neural crest (NC) arise at the dorsal aspect of the neural tube, then migrate throughout the developing embryo and differentiate into diverse cell types, including the sensory neurons and glia of the dorsal root ganglia (DRG). As multiple cell types are derived from this lineage, it is ideal for examining mechanisms of fate restriction during development. We have isolated a mutant, ouchless, that specifically fails to develop DRG neurons, although other NC derivatives develop normally. This mutation affects the expression of Sorbs3, a scaffold protein known to interact with proteins involved in focal adhesions and several signaling pathways. ouchless mutants share some phenotypic similarities with mutants in ErbB receptors, EGFR homologs that are implicated in diverse developmental processes and associated with several cancers; and ouchless interacts genetically with an allele of erbb3 in DRG neurogenesis. However, the defect in ouchless DRG neurogenesis is distinct from ErbB loss of function in that it is not associated with a loss of glia. Both ouchless and neurogenin1 heterozygous fish are sensitized to the effects of ErbB chemical inhibitors, which block the development of DRG in a dose-dependent manner. Inhibitors of MEK show similar effects on DRG neurogenesis. We propose a model in which Sorbs3 helps to integrate ErbB signals to promote DRG neurogenesis through the activation of MAPK and upregulation of neurogenin1.

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“…Therefore, the branching in Xphb1-dependent and -independent c-myc targets observed here is surprising and has not been reported previously. Depletion of the CNC specifiers sox10 and sox9, for example, results in loss of twist, foxD3, snail2 and snail1 expression (Honore et al, 2003;Lee et al, 2004;Spokony et al, 2002). More recently, a disjunctive regulation of snail1 and snail2 has been demonstrated in RhoVdepleted embryos.…”

Section: Discussionmentioning

confidence: 99%

Prohibitin1 acts as a neural crest specifier in Xenopus development by repressing the transcription factor E2F1

2010

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SUMMARYProhibitin 1 (phb1), which was initially described as an inhibitor of cell proliferation, is a highly conserved protein found in multiple cellular compartments. In the nucleus it interacts with the transcriptional regulators Rb and E2F1 and controls cell proliferation and apoptosis. Here we unravel an unexpected novel function for phb1 in Xenopus cranial neural crest (CNC) development. Xphb1 is maternally expressed; zygotically expressed neurula stage transcripts accumulate in the CNC and the neural tube. Knockdown of Xphb1 by antisense morpholino injection results in the loss of foxD3, snail2 and twist expression, whereas expression of c-myc, AP-2 and snail1 remains unaffected. Xphb2, its closest relative, cannot substitute for Xphb1, underlining the specificity of Xphb1 function. Epistatic analyses place Xphb1 downstream of c-myc and upstream of foxD3, snail2 and twist. To elucidate which subdomain in Xphb1 is required for neural crest gene regulation we generated deletion mutants and tested their rescue ability in Xphb1 morphants. The E2F1-binding domain was found to be necessary for Xphb1 function in neural crest development. Gain-and loss-of-function experiments reveal that Xphb1 represses E2F1 activity; suppression of E2F1 through Xphb1 is required for twist, snail2 and foxD3 expression in the CNC. With the Xphb1 dependency of a subset of CNC specifiers downstream of c-myc, we have identified a new branching point in the neural crest gene regulatory network.

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Early requirement of the transcriptional activator Sox9 for neural crest specification in Xenopus

Cited by 46 publications

References 46 publications

Evolution of the neural crest viewed from a gene regulatory perspective

Evolution of the neural crest viewed from a gene regulatory perspective

Modulation of dorsal root ganglion development by ErbB signaling and the scaffold protein Sorbs3

Prohibitin1 acts as a neural crest specifier in Xenopus development by repressing the transcription factor E2F1

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