FOXP2 belongs to a forkhead subfamily with transcription activity. Foxp2(R552H) knock-in (KI) mice with mutation related to the speech-language disorder exhibit abnormal dendrite development of Purkinje cells. To make clear the relationship between dendrite development of Purkinje cells and roles of FOXP2, we prepared Transgenic (Tg) mice that express human FOXP2-myc in Purkinje cells (Pcp2-FOXP2-myc-Tg mice). Heterozygous Pcp2-FOXP2-myc-Tg mice recovered their impaired USV, but homozygous ones did not. FOXP2 expression promoted dendrite formation in Purkinje cells. They exhibited the promoted dendrite formation in Purkinje cells and the enhanced intensity of GABAB2 receptor and VGluT1 immunoreactivities in the molecular layer. In the present study, we examined the gene expression regulated by FOXP2 in the cerebellum by Microarray and real-time quantitative PCR analyses. We focused trafficking protein particle complex 5 (Trappc5),that trafficking protein particle complex 5 (Trappc5), a constituents of TRAPP complex which is involved in Golgi trafficking, was up-regulated in the cerebellum of Pcp2-FOXP2-myc-Tg pups. In addition to Golgi, Trappc5 was partly localized to the ER and mitochondria in the dendrites of neurons and in the molecular layer in the cerebellum. The intensity of Trappc5 immunoreactivity was enhanced in their molecular layer. TRAPP complex containing Trappc5 may play a role in the Foxp2-mediated dendrite development of Purkinje cells.