Neural information processed through the striatum of the basal ganglia is crucial for sensorimotor and psychomotor functions. Genes that are highly expressed in the striatum during development may be involved in neural development and plasticity in the striatum. We report in the present study the identification of a previously uncharacterized mammalian member of the nocA/elB/tlp-1 family, Nolz-1, that is preferentially expressed at high levels in the developing striatum. Nolz-1 mRNA was expressed as soon as striatal anlage began to form at embryonic day 13 in the rat. Nolz-1 mRNA was predominantly expressed in the lateral ganglionic eminence (striatal primordium) and was nearly absent in the adjacent structures of the medial ganglionic eminence and the cerebral cortex. Moreover, Nolz-1 was highly expressed in the subventricular zone of the lateral ganglionic eminence and was colocalized with the early neuronal differentiation markers of TuJ1 and Isl1 and the projection neuron marker of DARPP-32, suggesting that Nolz-1 was expressed in differentiating progenitors of striatal projection neurons. A time course study showed that Nolz-1 mRNA was developmentally regulated, as its expression was down-regulated postnatally with low levels remaining in the ventral striatum at adulthood. As the tagged Nolz-1 protein was localized in the nucleus, Nolz-1 may function as transcriptional regulator. In a model system for neural differentiation, Nolz-1 mRNA was dramatically induced on neural induction of P19 embryonal carcinoma cells by retinoic acid, suggesting that Nolz-1 activation may be involved in neural differentiation. Our study suggests that Nolz-1 is preferentially expressed in differentiating striatal progenitors and may be engaged in the genetic program for controlling striatal development.
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Neural information processed through the striatum of the basal ganglia is crucial for sensorimotor and psychomotor functions. Genes that are highly expressed in the striatum during development may be involved in neural development and plasticity in the striatum. We report in the present study the identification of a previously uncharacterized mammalian member of the nocA/elB/tlp-1 family, Nolz-1, that is preferentially expressed at high levels in the developing striatum. Nolz-1 mRNA was expressed as soon as striatal anlage began to form at embryonic day 13 in the rat. Nolz-1 mRNA was predominantly expressed in the lateral ganglionic eminence (striatal primordium) and was nearly absent in the adjacent structures of the medial ganglionic eminence and the cerebral cortex. Moreover, Nolz-1 was highly expressed in the subventricular zone of the lateral ganglionic eminence and was colocalized with the early neuronal differentiation markers of TuJ1 and Isl1 and the projection neuron marker of DARPP-32, suggesting that Nolz-1 was expressed in differentiating progenitors of striatal projection neurons. A time course study showed that Nolz-1 mRNA was developmentally regulated, as its expression was down-regulated postnatally with low levels remaining in the ventral striatum at adulthood. As the tagged Nolz-1 protein was localized in the nucleus, Nolz-1 may function as transcriptional regulator. In a model system for neural differentiation, Nolz-1 mRNA was dramatically induced on neural induction of P19 embryonal carcinoma cells by retinoic acid, suggesting that Nolz-1 activation may be involved in neural differentiation. Our study suggests that Nolz-1 is preferentially expressed in differentiating striatal progenitors and may be engaged in the genetic program for controlling striatal development.
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skos:exactMatch | |
uniprot:name |
Proc. Natl. Acad. Sci. U.S.A.
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uniprot:author |
Chang C.W.,
Chen H.Y.,
Fann M.J.,
Hayashizaki Y.,
Li H.Y.,
Liu F.C.,
Saito T.,
Takahashi H.,
Tsai C.W.,
Tsai H.C.,
Tsai T.F.,
Wang H.F.,
Yang C.W.
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uniprot:date |
2004
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uniprot:pages |
2613-2618
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uniprot:title |
Identification of a developmentally regulated striatum-enriched zinc-finger gene, Nolz-1, in the mammalian brain.
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uniprot:volume |
101
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dc-term:identifier |
doi:10.1073/pnas.0308645100
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