Expression and regulation of vitamin D 3 upregulated protein 1 (VDUP1) is conserved in mammalian and insect brain
Originally characterized as a cell‐cycle inhibitor induced by vitamin D 3 , the tumor suppressor vitamin‐D 3 upregulated protein 1 (VDUP1) has increasingly been shown to play major physiological roles in cell differentiation and glucose metabolism. Here we show evolutionarily conserved expression pa...
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Veröffentlicht in: | Journal of comparative neurology (1911) 2009-12, Vol.517 (5), p.581-600 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Originally characterized as a cell‐cycle inhibitor induced by vitamin D
3
, the tumor suppressor vitamin‐D
3
upregulated protein 1 (VDUP1) has increasingly been shown to play major physiological roles in cell differentiation and glucose metabolism. Here we show evolutionarily conserved expression patterns of VDUP1 in
Drosophila
and rat nervous systems, including subcellular localization—cytoplasmic enrichment in neurons and nuclear expression in glia. These anatomical correlates suggested conservation of VDUP1 regulation, which was investigated both functionally and through promoter studies. Characterization of orthologous
vdup1 cis
‐regulatory regions identified evolutionarily conserved sequence blocks (CSBs) with similarities to neural enhancers, including basic helix‐loop‐helix (bHLH) transcription factor
Neurogenin/Math/atonal
and
Mash/achaete‐scute
family members. E‐boxes (CANNTG), the binding sites for bHLH proteins, were associated with these CSBs as well, including E‐boxes known to mediate glucose‐dependent upregulation of VDUP1 in nonneuronal cells. Hyperglycemia‐induced upregulation of VDUP1 was observed in brain tumor cells and in the
Drosophila
nervous system, which resulted in developmental arrest. Taken together, these data demonstrate evolutionary conservation of VDUP1 regulation and function, and suggest an expanding role for VDUP1 in nervous system development. J. Comp. Neurol. 517:581–600, 2009. © 2009 Wiley‐Liss, Inc. |
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ISSN: | 0021-9967 1096-9861 |
DOI: | 10.1002/cne.22195 |