PMID:18339674

Citation	Du, T, Xu, Q, Ocbina, PJ and Anderson, SA (2008) NKX2.1 specifies cortical interneuron fate by activating Lhx6. Development 135:1559-67
Abstract	In the ventral telencephalon, the medial ganglionic eminence (MGE) is a major source of cortical interneurons. Expression of the transcription factor NKX2.1 in the MGE is required for the specification of two major subgroups of cortical interneurons - those that express parvalbumin (PV) or somatostatin (SST) - but direct targets of NKX2.1 remain to be established. We find that electroporation of Nkx2.1 cDNA into the ventral telencephalon of slice cultures from Nkx2.1-/- mouse embryos, followed by transplantation into neonatal cortex to permit postnatal analysis of their fate, rescues the loss of PV- and SST-expressing cells. The LIM-homeobox gene Lhx6 is induced by this rescue experiment, and gain- and loss-of-function studies suggest that Lhx6 is necessary and sufficient to rescue these and other interneuron phenotypes in cells transplanted from Nkx2.1-/- slices. Finally, NKX2.1 protein binds a highly conserved sequence in the Lhx6 promoter, and this sequence appears to mediate the direct activation of Lhx6 by NKX2.1. The slice transfection and transplantation methods employed here are beginning to uncover embryonic mechanisms for specifying neuronal fates that only become definable postnatally.
Links	PubMed Online version:10.1242/dev.015123
Keywords	Animals; Base Sequence; Brain Tissue Transplantation; Cell Differentiation; Cerebral Cortex/cytology; Cerebral Cortex/embryology; Cerebral Cortex/metabolism; DNA Primers/genetics; Embryo Culture Techniques; Female; Gene Expression Regulation, Developmental; Homeodomain Proteins/antagonists & inhibitors; Homeodomain Proteins/genetics; Homeodomain Proteins/metabolism; Interneurons/cytology; Interneurons/metabolism; LIM-Homeodomain Proteins; Median Eminence/cytology; Median Eminence/embryology; Median Eminence/metabolism; Mice; Mice, Knockout; Mice, Transgenic; Nerve Tissue Proteins/antagonists & inhibitors; Nerve Tissue Proteins/genetics; Nerve Tissue Proteins/metabolism; Nuclear Proteins/deficiency; Nuclear Proteins/genetics; Nuclear Proteins/metabolism; Parvalbumins/genetics; Phenotype; Pregnancy; Promoter Regions, Genetic; RNA Interference; Somatostatin/genetics; Transcription Factors/deficiency; Transcription Factors/genetics; Transcription Factors/metabolism; Transfection
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