Back to basics: SOX genes

Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, Utah 84132, USA.
Developmental Dynamics (Impact Factor: 2.38). 08/2007; 236(8):2356-66. DOI: 10.1002/dvdy.21218
Source: PubMed


Sox genes are indispensable for multiple aspects of development. This primer briefly describes shared properties of the Sox gene family, and five well-characterized examples of vertebrate developmental mechanisms governed by Sox gene subgroups: testis development, central nervous system neurogenesis, oligodendrocyte development, chondrogenesis, and neural crest cell development. Also featured is an interview about current issues in the field with experts Jonas Muhr, Ph.D. and Robert Kelsh, Ph.D.

10 Reads
  • Source
    • "Acting alongside Notch signalling in bilaterians, SoxB genes are a subfamily of the HMG-box domain-containing Sox transcription factor family, the activities of which often concern the maintenance of stem cell identity versus regulated cellular differentiation [reviewed by Kiefer (2007)]. Diverse bilaterians express SoxB orthologues during early neurogenesis [e.g. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Notch signalling, SoxB and Group A bHLH 'proneural' genes are conserved regulators of the neurogenic program in many bilaterians. However, the ancestry of their functions and interactions is not well understood. We address this question in the sea anemone Nematostella vectensis, a representative of the Cnidaria, the sister clade to the Bilateria. It has previously been found that the SoxB orthologue NvSoxB(2) is expressed in neural progenitor cells (NPCs) in Nematostella and promotes the development of both neurons and nematocytes, whereas Notch signalling has been implicated in the negative regulation of neurons and the positive regulation of nematocytes. Here, we clarify the role of Notch by reporting that inhibition of Notch signalling increases the numbers of both neurons and nematocytes, as well as increasing the number of NvSoxB(2)-expressing cells. This suggests that Notch restricts neurogenesis by limiting the generation of NPCs. We then characterise NvAth-like (Atonal/Neurogenin family) as a positive regulator of neurogenesis that is co-expressed with NvSoxB(2) in a subset of dividing NPCs, while we find that NvAshA (Achaete-scute family) and NvSoxB(2) are co-expressed in non-dividing cells only. Reciprocal knockdown experiments reveal a mutual requirement for NvSoxB(2) and NvAth-like in neural differentiation; however, the primary expression of each gene is independent of the other. Together, these data demonstrate that Notch signalling and NvSoxB(2) regulate Nematostella neural progenitors via parallel yet interacting mechanisms; with different aspects of these interactions being shared with Drosophila and/or vertebrate neurogenesis.
    Development 10/2015; 142(142):3332-3342. DOI:10.1242/dev.123745 · 6.46 Impact Factor
  • Source
    • "The mechanism involving Sox17 in this regulation is still unclear. Sox transcription factors can bind specific DNA sequences but their mode of action depends on requisite partners for target specificity [35]. Through their ability to bind the minor groove of DNA, they can induce conformational changes that bring distant proteins on gene promoters closer together allowing their interaction. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Liver is a major regulator of lipid metabolism and adaptation to fasting, a process involving PPARalpha activation. We recently showed that the Vnn1 gene is a PPARalpha target gene in liver and that release of the Vanin-1 pantetheinase in serum is a biomarker of PPARalpha activation. Here we set up a screen to identify new regulators of adaptation to fasting using the serum Vanin-1 as a marker of PPARalpha activation. Mutagenized mice were screened for low serum Vanin-1 expression. Functional interactions with PPARalpha were investigated by combining transcriptomic, biochemical and metabolic approaches. We characterized a new mutant mouse in which hepatic and serum expression of Vanin-1 is depressed. This mouse carries a mutation in the HMG domain of the Sox17 transcription factor. Mutant mice display a metabolic phenotype featuring lipid abnormalities and inefficient adaptation to fasting. Upon fasting, a fraction of the PPARα-driven transcriptional program is no longer induced and associated with impaired fatty acid oxidation. The transcriptional phenotype is partially observed in heterozygous Sox17+/- mice. In mutant mice, the fasting phenotype but not all transcriptomic signature is rescued by the administration of the PPARalpha agonist fenofibrate. These results identify a novel role for Sox17 in adult liver as a modulator of the metabolic adaptation to fasting.
    PLoS ONE 08/2014; 9(8):e104925. DOI:10.1371/journal.pone.0104925 · 3.23 Impact Factor
    • "Therefore, other molecular aberrations are determining the course of the disease and novel markers are urgently needed to ensure an evidence-based personalized decision-making in these patients. SOX11, a member of the SRY-related HMG-box transcription factor family plays important biological roles in cell fate determination and differentiation [8] [9] and in embryonic neurogenesis and tissue remodeling [10] [11] [12] [13] and might constitute a new tool for diagnosing MCL. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Recent studies have identified SOX11 as a novel diagnostic marker for mantle cell lymphoma (MCL). We quantified SOX11 by a truly mRNA specific qPCR assay in longitudinal peripheral blood samples from 20 patients and evidenced a close relationship of SOX11 expression and clinical status of the patients. In eight patient courses we validated the expression of SOX11 using t(11;14) and demonstrated positive correlation of SOX11 and t(11;14) levels. To our knowledge this is the first report stating that quantification of SOX11 can be used as an minimal residual disease marker equal to the key translocation t(11;14) in MCL.
    Leukemia Research 08/2014; 38(8). DOI:10.1016/j.leukres.2014.04.007 · 2.35 Impact Factor
Show more