The human KAL gene is responsible for the X chromosome-linked Kallmann
syndrome, which consists of the association of hypogonadotropic hypog
onadism and anosmia. The human and chicken KAL genes have been isolate
d. Using in situ hybridization, we studied KAL gene expression during
development of the chick. We have previously reported that, from embry
onic day 8, the expression is almost restricted to definite neuronal p
opulations in the central nervous system, most of which still express
the gene after hatching. Here we report that the KAL gene is also expr
essed during early embryonic development (days 2-8) in various endoder
mal, mesodermal, and neurectodermal derivatives. In most endodermal an
d mesodermal derivatives, the expression is transient and precedes cel
l differentiation. In contrast, the expression in the nervous system c
oncerns postmitotic central neuroblastic populations, most of which st
ill express the gene after differentiation. In accordance with such a
spatio-temporal pattern of expression, we suggest that the KAL gene is
involved both in morphogenetic events and in neuronal late differenti
ation. In addition, the absence of detectable expression of the KAL ge
ne either in the embryonic olfactory epithelium or in the surrounding
nasal mesenchyme reinforces the hypothesis that Kallmann's syndrome re
sults from a central olfactory target cell defect.