Among the families of transcription factors expressed at the neural plate border in response to neural crest-inducing signals, Sox proteins have emerged as important players in regulating multiple aspects of neural crest development. Here, we summarize the expression of six Sox genes, namely Sox8, Sox9, Sox10, LSox5, Sox4 and Sox11, in neural crest progenitors and their derivatives, and review some aspects of their function pertaining to neural crest development in several species.
"Foxd3 is often thought of as a defining neural crest marker (Labosky and Kaestner, 1998; Sasai et al., 2001; Sauka- Spengler and Bronner-Fraser, 2008; Stewart et al., 2006), although as described above, it is also expressed in early pre-neural ectoderm , in the organizer and in epiblast and trophectoderm lineages in mice (Arduini and Brivanlou, 2012; Steiner et al., 2006; Tompers et al., 2005; Xu et al., 2009) and in the presumptive posterior neurectoderm in Xenopus (Sasai et al., 2001). Some of these genes such as Msx1/2 and Foxd3 will eventually localize with Pax3 or Pax7 to the developing neural folds where nascent neural crest cells will form, marked by the expression of Snail and SoxE family genes (Aoki et al., 2003; Betancur et al., 2010; Grocott et al., 2012; Hong and Saint-Jeannet, 2005; Lee et al., 2004; Milet and Monsoro-Burq, 2012). Others, such as Foxi1/3, Dlx5/6 and Gata2/3 will localize with pre-placodal region genes such as Six1/4 and Eya1/2 (Grocott et al., 2012). "
[Show abstract][Hide abstract] ABSTRACT: The neural crest and craniofacial placodes are two distinct progenitor populations that arise at the border of the vertebrate neural plate. This border region develops through a series of inductive interactions that begin before gastrulation and progressively divide embryonic ectoderm into neural and non-neural regions, followed by the emergence of neural crest and placodal progenitors. In this review, we describe how a limited repertoire of inductive signals - principally FGFs, Wnts and BMPs - set up domains of transcription factors in the border region which establish these progenitor territories by both cross-inhibitory and cross-autoregulatory interactions. The gradual assembly of different cohorts of transcription factors that results from these interactions is one mechanism to provide the competence to respond to inductive signals in different ways, ultimately generating the neural crest and cranial placodes.
"Once the neural plate border has been specified, SoxE family transcription factors are the earliest markers of the subset of these border cells competent to give rise to the definitive NC (Sauka-Spengler and Bronner-Fraser, 2008). In avians and mammals, Sox9 expression distinguishes NC precursor cells, whereas Sox8 does in Xenopus with Sox9 expression following soon after (Hong and Saint-Jeannet, 2005). Sox10 is expressed, or functions, somewhat later in NC precursors in most species and thus its predominant role may be in later regulatory events, particularly melanocyte and glia formation. "
[Show abstract][Hide abstract] ABSTRACT: Neural crest cells are the primary innovation that led to evolution of the vertebrates, and transcription factors of the SoxE family (Sox8, Sox9 and Sox10) are among the central players regulating the development of these cells. In all vertebrates examined to date, one or more SoxE proteins are required for the formation of neural crest cells, the maintenance of their multipotency, and their survival. Later, SoxE proteins drive the formation of multiple neural crest derivatives including chondrocytes, melanocytes, and cells of the peripheral nervous system, particularly Schwann cells/peripheral glia. Given their multiple diverse roles in the development of the neural crest, it is important to understand how the activity of SoxE factors is controlled such that they direct the correct developmental outcome. While combinatorial control with other regulatory factors is clearly one mechanism for generating such functional versatility, modulation of SoxE activity, both by SoxD family factors and by post-translational modification, also appears to be important. Elucidating the mechanisms that control SoxE function is essential to understand the evolutionary origin of the vertebrates, as well as a host of SoxE-linked syndromes and diseases, and may prove crucial for developing stem cell based therapies that target SoxE-regulated cell types.
The international journal of biochemistry & cell biology 11/2009; 42(3):441-4. DOI:10.1016/j.biocel.2009.11.014 · 4.05 Impact Factor
"Based on their homology within and outside this domain, Sox proteins have been classified into 10 groups (A-J) (Bowles et al., 2000). Members of Sox group E include Sox8, Sox9 and Sox10; in the recent years SoxE genes have been extensively studied for their role in chondrogenesis, sex determination, pigment cell differentiation, gliogenesis and neural crest development (reviewed by de Crombrugghe et al., 2001; Koopman, 2005; Wegner, 2005; Wegner and Stolt, 2005; Hong and Saint-Jeannet, 2005). "
[Show abstract][Hide abstract] ABSTRACT: Among the families of transcription factors expressed at the neural plate border, Sox proteins have been shown to regulate multiple aspects of neural crest development. Sox8, Sox9 and Sox10, exhibit overlapping expression domains in neural crest progenitors, and studies in mouse suggest that Sox8 functions redundantly with Sox9 and Sox10 during neural crest development. Here, we show that in Xenopus, Sox8 accumulates at the lateral edges of the neural plate at the mid-gastrula stage; in contrast to its mouse and chick orthologs, Sox8 expression precedes that of Sox9 and Sox10 in neural crest progenitors. Later in development, Sox8 expression persists in migrating cranial crest cells as they populate the pharyngeal arches and in trunk neural crest cells, in a pattern that recapitulates both Sox9 and Sox10 expression domains. Although morpholino-mediated knockdown of Sox8 protein did not prevent the formation of neural crest progenitors, the timing of their induction was severely affected. This delay in neural crest specification had dramatic consequences on the development of multiple lineages of the neural crest. We demonstrate that these defects are due to the inability of neural crest cells to migrate into the periphery, rather than to a deficiency in neural crest progenitors specification and survival. These results indicate that the control of Sox8 expression at the neural plate border is a key process in initiating neural crest formation in Xenopus, and highlight species-specific differences in the relative importance of SoxE proteins during neural crest development.
Development 11/2006; 133(19):3817-26. DOI:10.1242/dev.02558 · 6.46 Impact Factor
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