In this thesis I studied the expression pattern of Emx2OS, the antisense partner of the homeobox gene Emx2, in the developing mouse nervous system. Emx2OS was detectable in telencephalon, mammillary recess, mesencephalon, nasal pits and otic vesicle, all of them also expressing Emx2. Within dorsal telencephalon, Emx2OS peaked in post-mitotic neurons, specifically at the time when they completed radial migration and turned Emx2 off. Such pattern suggested that Emx2OS may be implicated in regulation of Emx2, according to complex and even antithetic ways. By artificially modulating Emx2OS in primary cortico-cerebral precursors, via lentiviral RNAi and somatic transgenesis, we found that such transcript contributes to down-regulation of its sense partner, possibly by a Dicer-dependent posttranscriptional mechanism. On the other side, by ectopically activating Emx2OS in primary rhombo-spinal precursors, we elicited a robust activation of Emx2. Further inspection of Emx2 null cortices conversely showed a collapse of Emx2OS expression. Taken together, these results suggest that a mutual positive loop involving Emx2 and Emx2OS is necessary to adequate expression of either transcript in the early neural tube.
|Titolo:||Regulation of Emx2 expression by antisense transcripts in the murine developing CNS|
|Data di pubblicazione:||22-ott-2009|
|Appare nelle tipologie:||8.1 PhD thesis|