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Abstract
During normal vertebrate development, Hoxd10 and Hoxd11 are expressed by differentiating
motoneurons in restricted patterns along the rostrocaudal axis of the lumbosacral
(LS) spinal cord. To assess the roles of these genes in the attainment of motoneuron
subtypes characteristic of LS subdomains, we examined subtype complement after overexpression
of Hoxd10 or Hoxd11 in the embryonic chick LS cord and in a Hoxd10 loss-of-function
mouse embryo. Data presented here provide evidence that Hoxd10 defines the position
of the lateral motor column (LMC) as a whole and, in rostral LS segments, specifically
promotes the development of motoneurons of the lateral subdivision of the lateral
motor column (LMCl). In contrast, Hoxd11 appears to impart a caudal and medial LMC
(LMCm) identity to some motoneurons and molecular profiles suggestive of a suppression
of LMC development in others. We also provide evidence that Hoxd11 suppresses the
expression of Hoxd10 and the retinoic acid synthetic enzyme, retinaldehyde dehydrogenase
2 (RALDH2). In a normal chick embryo, Hoxd10 and RALDH2 are expressed throughout the
LS region at early stages of motoneuron differentiation but their levels decline in
Hoxd11-expressing caudal LS segments that ultimately contain few LMCl motoneurons.
We hypothesize that one of the roles played by Hoxd11 is to modulate Hoxd10 and local
retinoic acid levels and thus, perhaps define the caudal boundaries of the LMC and
its subtype complement.