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Mutation of murine HoxaS has shown that HOXAS controls lung, gastrointestinal tract and vertebrae development. HoxaS is also expressed in the spinal cord, yet no central nervous system phenotype has been described in the HoxaS knockout mice. To identify the role of HOXA5 in the developing spinal cord, we produced transgenic mice that overexpress HoxaS mRNA in the brachial (C4-T2) spinal cord. Multiple founder transgenic mice and one established transgenic line (HoxaSSV2) show skin ulceration of the chest and forelimbs, in regions innervated by C4-C7 sensory neurons. In HoxaSSVl, transgenic mice also display forelimb specific motor and sensory defects. Transgenics cannot support their body weight in a hang test, and forelimb strength is decreased in a weight pull test. However, Rotarod performance was not impaired in HoxaSSV2 mice. HoxaSSVl mice also show a delayed forelimb response to noxious heat, although the hindlimb response time was normal. Interestingly, administration of an analgesic 47 eliminated the hang test defect, indicating that pain pathways are involved in this behavioral defect. The morphology of transgenic cervical (but not lumbar) spinal cord is highly aberrant. Nissl staining indicates Laminae 1 and 2 of the dorsal horn appear to be absent or severely reduced in the C4-C7 region only, overlapping with the set of sensory neurons innervating affected skin regions. The distribution of cells and axons immunoreactive for substance P and neurokinin-B as well as the neurokinin-1 and neurokinin-3 receptors were also dramatically altered only in transgenic brachial spinal cord, similar to the morphological changes seen. The general pattern of substance P immunoreactivity in axons innervating transgenic footpads and in dorsal root ganglia appeared to be normal. We conclude that, in this transgenic line, the development and possibly correct specification of dorsal intemeurons involved in nociception is disrupted.

Functional analysis of Hoxa5: analysis of structural, behavioral, and molecular effects of Hoxa5 overexpression in transgenic line Hoxa5SV2