Multiple non-cell-autonomous defects underlie neocortical callosal dysgenesis in Nfib-deficient mice.

ABSTRACT:

Background

Agenesis of the corpus callosum is associated with many human developmental syndromes. Key mechanisms regulating callosal formation include the guidance of axons arising from pioneering neurons in the cingulate cortex and the development of cortical midline glial populations, but their molecular regulation remains poorly characterised. Recent data have shown that mice lacking the transcription factor Nfib exhibit callosal agenesis, yet neocortical callosal neurons express only low levels of Nfib. Therefore, we investigate here how Nfib functions to regulate non-cell-autonomous mechanisms of callosal formation.

Results

Our investigations confirmed a reduction in glial cells at the midline in Nfib-/- mice. To determine how this occurs, we examined radial progenitors

SUBMITTER: Piper M 

PROVIDER: S-EPMC2802587 | biostudies-literature | 2009 Dec

REPOSITORIES: biostudies-literature