Deficiency of Kif15 impairing synaptic development leads to mood disorder in mice

The harmony of neuronal excitation and inhibition is essential for precise neuronal circuitry in the developmental brain, and thus affects the human emotion. Abnormalities of synaptic morphology directly affect neuronal function and contribute to a variety of psychiatric disorders. Previous studies have shown that Kif15 (Kinesin-12), a microtubule-associated motor protein, affects neurite growth, navigation, and branching during neuronal development, revealing the potential of Kif15 to influence neuronal dendritic morphology. A GWAS study in a European population showed that there were variants in both exons and introns of the KIF15 gene on chromosome 3 in patients with depression. Therefore, we generated Kif15-/- mice using CRISPR/Cas9 technology. In this study, we found that Kif15-/- mice have exhibited significant impacts on dendritic morphology and function, which contributes to mood disorders. Compared with Kif15 wild-type mice, adolescent Kif15-/- mice showed a significant decrease in the excitatory postsynaptic scaffolding protein PSD95 and NMDA receptors, as well as a reduction in the total density of dendritic spines and the density of mushroom spines, and a decrease in the frequency of mEPSCs. Meanwhile, the inhibitory postsynaptic scaffold protein Gephyrin and GABRB1 significantly upregulated. However, the adult Kif15-/- mice simultaneously exhibited an obvious manic behavior and their PSD95 expression increased rapidly, even more than that of the Kif15 wild-type mice. Meanwhile, overexpression of Kif15 in kif15-/- zebrafish rescued their depressive behavior. In terms of molecular mechanism, we showed that KIF15 interacted with PSD95 protein using both endogenous and exogenous Co-IP assays. Furthermore, we found that PSD95 in Kif15-/- mice was distributed around neuronal nuclei, in contrast to PSD95 localized close to the cell membrane in Kif15 wild-type mice. In conclusion, our study has identified a microtubule-associated molecular motor, KIF15, that plays a novel role in bipolar disorder through its contributions to spine morphology and function.

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Publication Details

Journal
PLoS Genetics
Published
2025-09-02
DOI
https://doi.org/10.1371/journal.pgen.1011839
Citations
1
Primary Topic
Microtubule and mitosis dynamics
Type
article
Field-Weighted Citation Impact
1.15

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article

Deficiency of Kif15 impairing synaptic development leads to mood disorder in mice

Zhangji Dong, Chao Wei, Tao Wu, Rongmei Kong et al.
1 citations
PLoS Genetics
Microtubule and mitosis dynamics
1.15
article

Deficiency of Kif15 impairing synaptic development leads to mood disorder in mice

Zhangji Dong, Chao Wei, Tao Wu, Rongmei Kong, Xiaomei He, Mei Liu, Ronghua Wu, Yan Liu, Xu Chen, Wei Zhang, Dexia Kong
article en
1 citations

Abstract

The harmony of neuronal excitation and inhibition is essential for precise neuronal circuitry in the developmental brain, and thus affects the human emotion. Abnormalities of synaptic morphology directly affect neuronal function and contribute to a variety of psychiatric disorders. Previous studies have shown that Kif15 (Kinesin-12), a microtubule-associated motor protein, affects neurite growth, navigation, and branching during neuronal development, revealing the potential of Kif15 to influence neuronal dendritic morphology. A GWAS study in a European population showed that there were variants in both exons and introns of the KIF15 gene on chromosome 3 in patients with depression. Therefore, we generated Kif15-/- mice using CRISPR/Cas9 technology. In this study, we found that Kif15-/- mice have exhibited significant impacts on dendritic morphology and function, which contributes to mood disorders. Compared with Kif15 wild-type mice, adolescent Kif15-/- mice showed a significant decrease in the excitatory postsynaptic scaffolding protein PSD95 and NMDA receptors, as well as a reduction in the total density of dendritic spines and the density of mushroom spines, and a decrease in the frequency of mEPSCs. Meanwhile, the inhibitory postsynaptic scaffold protein Gephyrin and GABRB1 significantly upregulated. However, the adult Kif15-/- mice simultaneously exhibited an obvious manic behavior and their PSD95 expression increased rapidly, even more than that of the Kif15 wild-type mice. Meanwhile, overexpression of Kif15 in kif15-/- zebrafish rescued their depressive behavior. In terms of molecular mechanism, we showed that KIF15 interacted with PSD95 protein using both endogenous and exogenous Co-IP assays. Furthermore, we found that PSD95 in Kif15-/- mice was distributed around neuronal nuclei, in contrast to PSD95 localized close to the cell membrane in Kif15 wild-type mice. In conclusion, our study has identified a microtubule-associated molecular motor, KIF15, that plays a novel role in bipolar disorder through its contributions to spine morphology and function.

PLoS GeneticsVol. 21(9)
Nantong University (CN), Nantong Science and Technology Bureau (CN)
National Natural Science Foundation of China, Nantong University
Openalex Percentile: Top 20%
Microtubule and mitosis dynamics
1.15
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