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Sall1 regulates mitral cell development and olfactory nerve extension in the developing olfactory bulb.

Authors :
Harrison SJ
Nishinakamura R
Monaghan AP
Source :
Cerebral cortex (New York, N.Y. : 1991) [Cereb Cortex] 2008 Jul; Vol. 18 (7), pp. 1604-17. Date of Electronic Publication: 2007 Nov 17.
Publication Year :
2008

Abstract

Sall1 is a zinc finger containing transcription factor that is highly expressed during mammalian embryogenesis. In humans, the developmental disorder Townes Brocks Syndrome is associated with mutations in the SALL1 gene. Sall1-deficient animals die at birth due to kidney deficits; however, its function in the nervous system has not been characterized. We examined the role of Sall1 in the developing olfactory system. We demonstrate that Sall1 is expressed by cells in the olfactory epithelium and olfactory bulb (OB). Sall1-deficient OBs are reduced in size and exhibit alterations in neurogenesis and mitral cell production. In addition, the olfactory nerve failed to extend past the ventral-medial region of the OB in Sall1-deficient animals. We observed intrinsic patterns of neurogenesis during olfactory development in control animals. In Sall1-mutant animals, these patterns of neurogenesis were disrupted. These findings suggest a role for Sall1 in regulating neuronal differentiation and maturation in developing neural structures.

Details

Language :
English
ISSN :
1460-2199
Volume :
18
Issue :
7
Database :
MEDLINE
Journal :
Cerebral cortex (New York, N.Y. : 1991)
Publication Type :
Academic Journal
Accession number :
18024993
Full Text :
https://doi.org/10.1093/cercor/bhm191