The Sox9 transcription factor determines glial fate choice in the developing spinal cord.
By C. Stolt, P. Lommes, E. Sock, Marie-Christine Chaboissier, A. Schedl, M. Wegner. Genes & Development, 2003
650 citations recorded by the source corpus.
The mechanism that causes neural stem cells in the central nervous system to switch from neurogenesis to gliogenesis is poorly understood. Here we analyzed spinal cord development of mice in which the transcription factor Sox9 was specifically ablated from neural stem cells by the CRE/loxP recombination system. These mice exhibit defects in the specification of oligodendrocytes and astrocytes, the two main types of glial cells in the central nervous system. Accompanying an early dramatic reduction in progenitors of the myelin-forming oligodendrocytes, there was a transient increase in motoneurons. Oligodendrocyte progenitor numbers recovered at later stages of development, probably owing to compensatory actions of the related Sox10 and Sox8, both of which overlap with Sox9 in the oligodendrocyte lineage. In agreement, compound loss of Sox9 and Sox10 led to a further decrease in oligodendrocyte progenitors. Astrocyte numbers were also severely reduced in the absence of Sox9 and did not recover at later stages of spinal cord development. Taking the common origin of motoneurons and oligodendrocytes as well as V2 interneurons and some astrocytes into account, stem cells apparently fail to switch from neurogenesis to gliogenesis in at least two domains of the ventricular zone, indicating that Sox9 is a major molecular component of the neuron-glia switch in the developing spinal cord.
Subfields: Developmental Neuroscience, Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/2fe104a296d66305ae52b09418c461327526ae10
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In Developmental Neuroscience
In Genetics
In Molecular Biology
- Hans Clevers
- M. van de Wetering
- Danish H Sayed
- A. Molofsky
- D. Rowitch
- B. Barres
- M. Abdellatif
- R. Nusse
Citations in the corpus
- SOX9 is an intestine crypt transcription factor, is regulated by the Wnt pathway, and represses the CDX2 and MUC2 genes (2004, background): “, 2003), cell commitment (Mori-Akiyama et al., 2003; Stolt et al., 2003), and differentiation (Kamachi et al.”
- Astrocytes and disease: a neurodevelopmental perspective. (2012, background): “Conditional knockout of Sox9 in the developing mouse spinal cord via nestin-cre (Stolt et al. 2003) led to an extended period of neurogenesis coupled with a significant delay in the onset of gliogenesis.”
- Physiology of Astroglia. (2018, neutral): “5 in the spinal cord and around E16–18 in the cortex; the onset is controlled by the transcription factors nuclear factor I-A (NFIA) (410) and Sox 9 that acts in association with NFIA (827, 1675), by Notch signaling, or by the transcriptional repressor N-CoR.”
- Somatic sex reprogramming of adult ovaries to testes by FOXL2 ablation. (2009, positive): “SOX9 was detected using an antibody described in Stolt et al. (2003) diluted 1:200.”
- MicroRNAs in development and disease. (2011, background): “Another highly relevant target is Sox9, which is known to be involved in promoting glial cell specification (581).”