Previous studies have defined a requirement for Sonic hedgehog (Shh) signaling in patterning the ventral telencephalon, a major source of the neuronal diversity found in the mature telencephalon. The zinc finger transcription factor Gli3 is a critical component of the Shh signaling pathway and its loss causes major defects in telencephalic development.Gli3is expressed in a graded manner along the dorsoventral axis of the telencephalon but it is unknown whetherGli3expression levels are important for dorsoventral telencephalic patterning. To address this, we used theGli3hypomorphic mouse mutantPolydactyly Nagoya(Pdn). We show that inPdn/Pdnembryos, the telencephalic expression ofGli3remains graded, butGli3mRNA and protein levels are reduced, resulting in an upregulation ofShhexpression and signaling. These changes mainly affect the development of the lateral ganglionic eminence (LGE), with some disorganization of the medial ganglionic eminence mantle zone. The pallial/subpallial boundary is shifted dorsally and the production of postmitotic neurons is reduced. Moreover, LGE pioneer neurons that guide corticofugal axons into the LGE do not form properly, delaying the entry of corticofugal axons into the ventral telencephalon.Pdn/Pdnmutants also show severe pathfinding defects of thalamocortical axons in the ventral telencephalon. Transplantation experiments demonstrate that the intrinsic ability of thePdnventral telencephalon to guide thalamocortical axons is compromised. We conclude that correctGli3levels are particularly important for the LGE's growth, patterning, and development of axon guidance capabilities.