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Background    Emx2  encodes for a transcription factor expressed in the embryonic intermediate mesoderm and central nervous system (CNS). It is implicated in several aspects of cerebral cortex development, including morphogenetic field specification, arealization, precursor proliferation and lamination. Four  Emx2 -associated antisense transcripts have been found in the urogenital system; one of them,  Emx2OS , has been also detected in the adult brain. Until now, however, nothing is known about expression and function of  Emx2OS  in the developing CNS.    Methodology/Principal Findings  By quantitative RT-PCR and in situ hybridization, we reconstructed the  Emx2OS  expression profile in the embryonic CNS, paying special attention to the developing cerebral cortex.  Emx2OS  was observed in a number of CNS structures expressing also  Emx2 . Within the cortex,  Emx2OS  was detectable in periventricular precursors, expressing the sense transcript, and peaked in newly born post-mitotic neurons not expressing such transcript. By integrating lentiviral gene delivery, RNAi, TetON technology, morpholino-mediated gene knock-down, drug-induced perturbation of gene expression, and quantitative RT-PCR, we addressed possible roles of  Ex2  antisense RNA in  Emx2  regulation, in primary CNS precursor cultures. We found that, in both cortical precursors and their neuronal progenies,  Emx2  antisense RNA contributes to post-transcriptional down-regulation of its sense partner, possibly by a Dicer-promoted mechanism. The same RNA, when delivered to rhombo-spinal precursors, stimulates ectopic expression of  Emx2 , whereas  Emx2  knock-out dramatically impairs  Emx2OS  transcription. This suggests that, within the developing CNS, a reciprocal  Emx2 / Emx2OS  regulatory loop may normally sustain transcription at the  Emx2  locus.    Conclusions/Significance  This study shows that antisense transcripts may contribute to developmental regulation of a key transcription factor gene implicated in CNS patterning, possibly by complex and multilevel mechanisms. The activation of  Emx2  by a short antisense transcript may be a prototype of a method for overexpressing  single specific  genes, without introducing additional copies of them into the genome.

Regulation of Emx2 Expression by Antisense Transcripts in Murine Cortico-Cerebral Precursors