| First Author | Park J | Year | 2019 |
| Journal | Mol Brain | Volume | 12 |
| Issue | 1 | Pages | 58 |
| PubMed ID | 31221192 | Mgi Jnum | J:289880 |
| Mgi Id | MGI:6435078 | Doi | 10.1186/s13041-019-0480-1 |
| Citation | Park J, et al. (2019) Inositol polyphosphate multikinase deficiency leads to aberrant induction of synaptotagmin-2 in the forebrain. Mol Brain 12(1):58 |
| abstractText | Inositol polyphosphate multikinase (IPMK), the key enzyme responsible for the synthesis of higher inositol polyphosphates and phosphatidylinositol 3, 4, 5-trisphosphate, is known to mediate various biological events, such as cellular growth and metabolism. Conditional deletion of IPMK in excitatory neurons of the mouse postnatal forebrain results in enhanced extinction of fear memory accompanied by activation of p85 S6 kinase 1 signaling in the amygdala; it also facilitates hippocampal long-term potentiation. However, the molecular changes triggered by IPMK deletion in the brain have not been fully elucidated. In the present study, we investigated gene expression changes in the hippocampal region of IPMK conditional knockout (cKO) mice by performing genome-wide transcriptome analyses. Here we show that expression of synaptotagmin 2 (Syt2), a synaptic vesicle protein essential for Ca(2+)-dependent neurotransmitter release, is robustly upregulated in the forebrain of IPMK(cKO) mice. Compared to wild-type mice, in which weak Syt2 expression was detected in the forebrain, IPMK(cKO) mice showed marked increases in both Syt2 mRNA and protein expression in the hippocampus as well as the amygdala. Collectively, our results suggest a physiological role for IPMK in regulating expression of Syt2, providing a potential underlying molecular mechanism to explain IPMK-mediated neural functions. |
