Abnormal development of forebrain midline glia and commissural projections in Nfia knock-out mice

Shu, Tianzhi, Butz, Kenneth G., Plachez, Celine, Gronostajski, Richard M. and Richards, Linda J. (2003) Abnormal development of forebrain midline glia and commissural projections in Nfia knock-out mice. Journal of Neuroscience, 23 1: 203-212.


Author Shu, Tianzhi
Butz, Kenneth G.
Plachez, Celine
Gronostajski, Richard M.
Richards, Linda J.
Title Abnormal development of forebrain midline glia and commissural projections in Nfia knock-out mice
Journal name Journal of Neuroscience  (ERA 2012 Listed)    (ERA 2010 Rank A*)   Check publisher's open access policy
Publication date 2003-01
Sub-type Article
Volume number 23
Issue number 1
ISSN 0270-6474; 1529-2401
Start page 203
End page 212
Total pages 10
Place of publication Washington
Publisher Soc Neuroscience
Language eng
Subject 1109 Neurosciences
Abstract Nuclear factor I (NFI) genes are expressed in multiple organs throughout development (Chaudhry et al., 1997; for review, see Gronostajski, 2000). All four NFI genes are expressed in embryonic mouse brain, with Nfia, Nfib, and Nfix being expressed highly in developing cortex (Chaudhry et al., 1997). Disruption of the Nfia gene causes agenesis of the corpus callosum (ACC), hydrocephalus, and reduced GFAP expression (das Neves et al., 1999). Three midline structures, the glial wedge, glia within the indusium griseum, and the glial sling are involved in development of the corpus callosum (Silver et al., 1982; Silver and Ogawa, 1983; Shu and Richards, 2001). Because Nfia(-/-) mice show glial abnormalities and ACC, we asked whether defects in midline glial structures occur in Nfia(-/-) mice. NFI-A protein is expressed in all three midline populations. In Nfia(-/-) mice sling cells are generated but migrate abnormally into the septum and do not form a sling. Glia within the indusium griseum and the glial wedge are greatly reduced or absent and consequently Slit2 expression is also reduced. Although callosal axons approach the midline, they fail to cross and extend aberrantly into the septum. The hippocampal commissure is absent or reduced, whereas the ipsilaterally projecting perforating axons (Hankin and Silver, 1988; Shu et al., 2001) appear relatively normal. These results support an essential role for midline glia in callosum development and a role for Nfia in the formation of midline glial structures.
Keyword Neurosciences
glial wedge
glial sling
glial tunnel
corpus callosum
anterior commissure
hippocampal commissure
Slit2
Nuclear Factor-i
Corpus-callosum
Binding Protein
Anterior Commissure
Gene-expression
Dna-replication
Adenovirus Dna
Mouse Strains
Optic Chiasm
Axon Tracts
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article
Collections: Excellence in Research Australia (ERA) - Collection
School of Biomedical Sciences Publications
 
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