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Tytuł pozycji:

Neuronal migration and ventral subtype identity in the telencephalon depend on SOX1

Tytuł :
Neuronal migration and ventral subtype identity in the telencephalon depend on SOX1
Autorzy :
Antigoni Ekonomou
Ilias Kazanis
Stavros Malas
Heather Wood
Pavlos Alifragis
Myrto Denaxa
Domna Karagogeos
Andrew Constanti
Robin Lovell-Badge
Vasso Episkopou
Pokaż więcej
Temat :
Faculty of Science\Biological Science
Animals Cell Movement/genetics Corpus Striatum/*physiology DNA-Binding Proteins/deficiency/genetics/*physiology Gene Deletion Genetic Vectors High Mobility Group Proteins/deficiency/genetics/*physiology Mice Mice
nervous system
Biology (General)
QH301-705.5
Knockout Molecular Sequence Data Neurons/*physiology Restriction Mapping SOXB1 Transcription Factors Sex-Determining Region Y Protein/genetics Telencephalon/*physiology
Źródło :
PLoS Biology, Vol 3, Iss 6, p e186 (2005)
PLoS Biology, 3 (6), Article e186. (2005)
Wydawca :
Public Library of Science (PLoS), 2005.
Rok publikacji :
2005
Kolekcja :
DOAJ-Articles_enriched
UCL_Discovery
DOAJ-Articles
UCL_Discovery_enriched
Opis pliku :
application/pdf; text
Język :
English
ISSN :
1545-7885
1544-9173
DOI :
10.1371/journal.pbio.0030186
Numer akcesji :
edsair.dedup.wf.001..45f4a23cf746f5da763f81fdf64c8255
Little is known about the molecular mechanisms and intrinsic factors that are responsible for the emergence of neuronal subtype identity. Several transcription factors that are expressed mainly in precursors of the ventral telencephalon have been shown to control neuronal specification, but it has been unclear whether subtype identity is also specified in these precursors, or if this happens in postmitotic neurons, and whether it involves the same or different factors. SOX1, an HMG box transcription factor, is expressed widely in neural precursors along with the two other SOXB1 subfamily members, SOX2 and SOX3, and all three have been implicated in neurogenesis. SOX1 is also uniquely expressed at a high level in the majority of telencephalic neurons that constitute the ventral striatum (VS). These neurons are missing in Sox1-null mutant mice. In the present study, we have addressed the requirement for SOX1 at a cellular level, revealing both the nature and timing of the defect. By generating a novel Sox1-null allele expressing beta-galactosidase, we found that the VS precursors and their early neuronal differentiation are unaffected in the absence of SOX1, but the prospective neurons fail to migrate to their appropriate position. Furthermore, the migration of non-Sox1-expressing VS neurons (such as those expressing Pax6) was also affected in the absence of SOX1, suggesting that Sox1-expressing neurons play a role in structuring the area of the VS. To test whether SOX1 is required in postmitotic cells for the emergence of VS neuronal identity, we generated mice in which Sox1 expression was directed to all ventral telencephalic precursors, but to only a very few VS neurons. These mice again lacked most of the VS, indicating that SOX1 expression in precursors is not sufficient for VS development. Conversely, the few neurons in which Sox1 expression was maintained were able to migrate to the VS. In conclusion, Sox1 expression in precursors is not sufficient for VS neuronal identity and migration, but this is accomplished in postmitotic cells, which require the continued presence of SOX1. Our data also suggest that other SOXB1 members showing expression in specific neuronal populations are likely to play continuous roles from the establishment of precursors to their final differentiation.

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