|
pubmed:abstractText |
Sall3 is a zinc finger containing putative transcription factor and a member of the Sall gene family. Members of the Sall gene family are highly expressed during development. Sall3-deficient mice die in the perinatal period because of dehydration and display alterations in palate formation and cranial nerve formation (Parrish et al. [2004] Mol Cell Biol 24:7102-7112). We examined the role of Sall3 in the development of the olfactory system. We determined that Sall3 is expressed by cells in the olfactory epithelium and olfactory bulb. Sall3 deficiency specifically alters formation of the glomerular layer. The glomerular layer was hypocellular, because of a decrease in the number of interneurons. The lateral ganglionic eminence and rostral migratory stream developed normally in Sall3-deficient animals, which suggests that Sall3 is not required for the initial specification of olfactory bulb interneurons. Fewer GAD65/67-, Pax6-, calretinin-, and calbindin-positive cells were detected in the glomerular layer, accompanied by an increase in cells positive for these markers in the granule cell layer. In addition, a complete absence of tyrosine hydroxylase expression was observed in the olfactory bulb in the absence of Sall3. However, expression of Nurr1, a marker of dopaminergic precursors, was maintained, indicating that dopaminergic precursors were present. Our data suggest that Sall3 is required for the terminal maturation of neurons destined for the glomerular layer.
|
