The molecular mechanisms regulating neurogenesis involve the control of gene expression by transcription factors.
Gbx1 and
Gbx2, two members of the Gbx family of homeodomain-containing transcription factors, are known for their essential roles in central nervous system development. The expression domains of
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The molecular mechanisms regulating neurogenesis involve the control of gene expression by transcription factors.
Gbx1 and
Gbx2, two members of the Gbx family of homeodomain-containing transcription factors, are known for their essential roles in central nervous system development. The expression domains of mouse
Gbx1 and
Gbx2 include regions of the forebrain, anterior hindbrain, and spinal cord. In the spinal cord,
Gbx1 and
Gbx2 are expressed in PAX2
+ interneurons of the dorsal horn and ventral motor neuron progenitors. Based on their shared domains of expression and instances of overlap, we investigated the functional relationship between
Gbx family members in the developing spinal cord using
Gbx1−/−,
Gbx2−/−, and
Gbx1−/−/
Gbx2−/− embryos. In situ hybridization analyses of embryonic spinal cords show upregulation of
Gbx2 expression in
Gbx1−/− embryos and upregulation of
Gbx1 expression in
Gbx2−/− embryos. Additionally, our data demonstrate that
Gbx genes regulate development of a subset of PAX2
+ dorsal inhibitory interneurons. While we observe no difference in overall proliferative status of the developing ependymal layer, expansion of proliferative cells into the anatomically defined mantle zone occurs in
Gbx mutants. Lastly, our data shows a marked increase in apoptotic cell death in the ventral spinal cord of
Gbx mutants during mid-embryonic stages. While our studies reveal that both members of the
Gbx gene family are involved in development of subsets of PAX2
+ dorsal interneurons and survival of ventral motor neurons,
Gbx1 and
Gbx2 are not sufficient to genetically compensate for the loss of one another. Thus, our studies provide novel insight to the relationship harbored between
Gbx1 and
Gbx2 in spinal cord development.
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