Disruption of Early Events in Thalamocortical Tract Formation in Mice Lacking the Transcription Factors Pax6 or Foxg1

摘要: Early events in the formation of thalamocortical tract remain poorly understood. Recent work has suggested that axons follow a path pioneered by transient thalamic afferents originating from medial part ventral telencephalon. We studied development these and mutant mice lacking transcription factors normally expressed dorsal thalamus or Pax6 is thalamus, but not telencephalon, fails to form −/− embryos. found telencephalon do Pax6−/− embryos; this may contribute failure their development. The distribution cells ↔ Pax6+/+ chimeras supports conclusions drawn forebrain marker gene expression required for normal thalamus. Failure afferent pathway develop therefore likely cell nonautonomous defect reflecting primary defects then examined efferents Foxg1−/− embryos, which lack recognizable telencephalic structures. In embryos navigate correctly through fail turn laterally into whereas other are able cross diencephalic/telencephalic boundary. Our results support role guiding early identify new factor regulating ability attract afferents.