Tokai Univ. School of Med. Molecular Life Sciences

Kajiwara K

Kajiwara, Kagemasa Dental MD Ph.D

Research Unit

The Latest Work


Abnormal gait, reduced locomotor activity and impaired motor coordination in Dgcr2-deficient mice.

It has been suggested that the DGCR2 gene plays a role in the pathogenesis of 22q11.2 deletion syndrome. To analyze its function, we used our Dgcr2-knock-out/EGFP-knock-in mice (Dgcr2-KO mice). At 20-26 weeks of age, approximately 20% of Dgcr2-KO mice showed gait abnormalities with trembling and difficulty to balance. Footprint test revealed awkward movements in Dgcr2-KO mice soon after they were placed on the floor. Once they started walking, their stride lengths were not different from wild-type mice. During initial 5 minutes after put in a new environment in the short-term open field test, Dgcr2-KO mice travelled significantly shorter distance and walked more slowly than wild-type mice. In addition, Dgcr2-KO mice revealed reduced cage activity compared to wild-type mice on the first day in the long-term open field test, whereas no significant difference after that. Dgcr2-KO mice also showed reduced latency to fall on Rotarod test and no improvement during training for 3 days. In histology, sparseness of cerebellar Purkinje cells was observed in Dgcr2-KO mice. Our results suggest that DGCR2 plays roles for motor control related to Purkinje cell function and that deficiency of DGCR2 in patients of 22q11.2 deletion syndrome could contribute to at least a part of their symptoms.

Please refer to the following article for further information.

Mugikura, S. et al., Biochemistry and BiophysicsReports 5 (2016) 120–126.

Immunostaining of the cerebellum from in wild-type and Dgcr2-KO mice using anti ▀III tubulin. The number of Purkinje cells appeared reduced in Dgcr2-KO mice compared to that in wild-type mice. The scale bar represents 100 Ám.