Vrk2 deficiency elicits aggressive behavior in female zebrafish
Ryohei Umeda, Hitoshi Teranishi, Kazumasa Hada, Nobuyuki Shimizu, Hiroshi Shiraishi, Hirotaro Urushibata, Shaohong Lai, Masahito Shide, Magdeline E. Carrasco Apolinario, Ryoko Higa, Kenshiro Shikano, Toshitaka Shin, Hiromitsu Mimata, Takatoshi Hikida, Toshikatsu Hanada, Reiko Hanada
Abstract
Abstract Vaccinia‐related kinase 2 (VRK2) is a serine/threonine kinase initially identified in highly proliferative cells such as thymocytes and fetal liver cells, and it is involved in cell proliferation and survival. VRK2 is also expressed in the brain; however, its molecular function in the central nervous system is mostly unknown. Many genome‐wide association studies (GWASs) have reported that VRK2 is a potential candidate molecule for neuropsychiatric diseases such as schizophrenia in humans. However, the pathophysiological relationship between VRK2 and neuropsychiatric disorders has not been fully investigated. In this study, we evaluated vrk2 ‐deficient ( vrk2 −/− ) zebrafish and found that vrk2 −/− female zebrafish showed aggressive behavior and different social preference compared with control ( vrk2 +/+ ) zebrafish, with low gamma‐aminobutyric acid (GABA) content in the brain and high density of neuronal dendrites when compared to vrk2 +/+ zebrafish. These findings suggest that female vrk2 −/− zebrafish were indeed a model of malbehavior characterized by aggression and social interaction, which can be attributed to the low levels of GABA content in their brain.