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© 1994 Oxford University Press

RESEARCH-ARTICLE

Expression of the Kallmann syndrome gene in human fetal brain and in the manipulated chick embryo

Beat Lutz, Shigeru Kuratani, Elena I. Rugarli1, Stefan Wawersik, Calvin Wong, Frederick R. Bieber2, Andrea Ballabio1,* and Gregor Eichele

Departments of Biochemistry, Baylor College of Medicine Houston, TX 77030 1Molecular and Human Genetics, Baylor College of Medicine Houston, TX 77030 2Department of Pathology, Brigham and Women's Hospital and Harvard Medical School Boston, MA 02115, USA

*To whom correspondence should be addressed

Received May 25, 1994; Revised August 2, 1994; Accepted August 2, 1994

Kallmann syndrome is an inherited disorder characterized by an abnormality in olfactory system development. The gene for the X-linked form of this disorder (KAL) maps to Xp22.3 and encodes a protein sharing homologies with molecules involved in neuronal migration and axonal pathfinding. Here we report the expression pattern of the KAL gene in various parts of the human fetal brain. We found KAL transcripts in granule cells of the olfactory bulb and the cerebellum, in the dorsomedial thalamus and in the developing cerebral cortex. To determine whether or not signals from the olfactory nerve are required for KAL expression in the olfactory bulb, we analyzed chick embryos in which the olfactory placode was surgically removed. Those embryos lacking an olfactory nerve had a histologically abnormal bulb which nevertheless expressed the KAL gene at high levels. These findings indicate that, while the development of the proper cytoarchitecture of the olfactory bulb requires the innervation by olfactory axons, the expression of KAL is independent of such developmental processes.


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