DBZ Regulates Cortical Cell Positioning and Neurite Development by Sustaining the Anterograde Transport of Lis1 and DISC1 through Control of Ndel1 Dual-Phosphorylation

Okamoto, Masanori; Iguchi, Takuma; Hattori, Tsuyoshi; Matsuzaki, Shinsuke; Koyama, Yoshihisa; Taniguchi, Manabu; Komada, Munekazu; Xie, Min; Yagi, Hideshi; Shimizu, Shoko; Konishi, Yoshiyuki; Omi, Minoru; Yoshimi, Tomohiko; Tachibana, Taro; Fujieda, Shigeharu; Katayama, Taiichi; Ito, Akira; Hirotsune, Shinji; Tohyama, Masaya; Sato, Makoto

doi:10.1523/jneurosci.5029-13.2015

Cited by 21 publications

(17 citation statements)

References 56 publications

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“…In utero electroporation. In utero electroporation was performed on E14.5 embryos from timed-pregnant WT ICR mice (SLC, Shizuoka, Japan) 57 . The pregnant mice were anesthetized by intraperitoneal injections with a solution containing 0.3 mg medetomidine (Domitor, Zenoaq Nippon Zenyaku Kogyo, Fukushima, Japan), 4 mg midazolam (Dormicum, Astellas Pharma Inc., Tokyo, Japan), and 5 mg butorphanol (Bettlefar, MP AGRO Co., Ltd., Hokkaido, Japan) per kg.…”

Section: Controlmentioning

confidence: 99%

Pathogenic POGZ mutation causes impaired cortical development and reversible autism-like phenotypes

et al. 2020

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Pogo transposable element derived with ZNF domain (POGZ) has been identified as one of the most recurrently de novo mutated genes in patients with neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD), intellectual disability and White-Sutton syndrome; however, the neurobiological basis behind these disorders remains unknown. Here, we show that POGZ regulates neuronal development and that ASD-related de novo mutations impair neuronal development in the developing mouse brain and induced pluripotent cell lines from an ASD patient. We also develop the first mouse model heterozygous for a de novo POGZ mutation identified in a patient with ASD, and we identify ASD-like abnormalities in the mice. Importantly, social deficits can be treated by compensatory inhibition of elevated cell excitability in the mice. Our results provide insight into how de novo mutations on high-confidence ASD genes lead to impaired mature cortical network function, which underlies the cellular pathogenesis of NDDs, including ASD.

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Section: Controlmentioning

confidence: 99%

Pathogenic POGZ mutation causes impaired cortical development and reversible autism-like phenotypes

et al. 2020

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“…The G‐protein‐independent pathway is primarily involved in neurite outgrowth . DISC1 is transported from neuronal soma to the neurite tips via suppression of GSK3β activity to regulate neurites …”

Section: Antipsychotic Drug‐targeted Receptors Regulate Neurites In Smentioning

confidence: 99%

“…An early study showed that a low dose of D2R agonist stimulated neurite outgrowth . However, when there is hyperdopaminergic D2R activation, D2R and DISC1 form a protein complex, which could limit transportation of DISC1 to neurite tips and decreases GSK3α‐Ser21 phosphorylation and GSK3β‐Ser9 phosphorylation, ultimately reducing microtubule elongation in neurites (Figure A and B) . D2R hyperactivity may be induced by an overstimulation of dopamine since there is increased presynaptic dopamine in the schizophrenia brain.…”

Section: Antipsychotic Drug‐targeted Receptors Regulate Neurites In Smentioning

confidence: 99%

Effects of antipsychotic drugs on neurites relevant to schizophrenia treatment

Huang

Song

2018

Medicinal Research Reviews

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Although antipsychotic drugs are mainly used for treating schizophrenia, they are widely used for treating various psychiatric diseases in adults, the elderly, adolescents and even children. Today, about 1.2% of the worldwide population suffers from psychosis and related disorders, which translates to about 7.5 million subjects potentially targeted by antipsychotic drugs. Neurites project from the cell body of neurons and connect neurons to each other to form neural networks. Deficits in neurite outgrowth and integrity are implicated in psychiatric diseases including schizophrenia. Neurite deficits contribute to altered brain development, neural networking and connectivity as well as symptoms including psychosis and altered cognitive function. This review revealed that (1) antipsychotic drugs could have profound effects on neurites, synaptic spines and synapse, by which they may influence and regulate neural networking and plasticity; (2) antipsychotic drugs target not only neurotransmitter receptors but also intracellular signaling molecules regulating the signaling pathways responsible for neurite outgrowth and maintenance; (3) high doses and chronic administration of antipsychotic drugs may cause some loss of neurites, synaptic spines, or synapsis in the cortical structures. In addition, confounding effects causing neurite deficits may include elevated inflammatory cytokines and antipsychotic drug-induced metabolic side effects in patients on chronic antipsychotic therapy. Unraveling how antipsychotic drugs affect neurites and neural connectivity is essential for improving therapeutic outcomes and preventing aversive effects for patients on antipsychotic drug treatment.

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“…Plasmids for EGFP-tubulin (#30487, gift from Tso-Pang Yao), mCherry-tubulin (#26768, gift from Torsten Wittmann), tdTomato-EB3 (#58090, gift from Michael Davidson) and pLifeAct-mTurquoise2 (#36201, gift from Dorus Gadella), were obtained from Addgene. Plasmids for EGFP-EB3, K5H-EGFP and dominant-negative Kif5s were as described previously (Konishi and Setou, 2009;Okamoto et al, 2015). K5H-mCherry was constructed by inserting the K5H sequence into pmCherry-N vector (BD Biosciences, Franklin Lakes, NJ).…”

Section: Transfectionmentioning

confidence: 99%

Kinesin-1 sorting in axons controls the differential retraction of arbor terminals

Seno

Ikeno

Mennya

et al. 2016

Journal of Cell Science

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The ability of neurons to generate multiple arbor terminals from a single axon is crucial for establishing proper neuronal wiring. Although growth and retraction of arbor terminals are differentially regulated within the axon, the mechanisms by which neurons locally control their structure remain largely unknown. In the present study, we found that the kinesin-1 (Kif5 proteins) head domain (K5H) preferentially marks a subset of arbor terminals. Time-lapse imaging clarified that these arbor terminals were more stable than others, because of a low retraction rate. Local inhibition of kinesin-1 in the arbor terminal by chromophore-assisted light inactivation (CALI) enhanced the retraction rate. The microtubule turnover was locally regulated depending on the length from the branching point to the terminal end, but did not directly correlate with the presence of K5H. By contrast, F-actin signal values in arbor terminals correlated spatiotemporally with K5H, and inhibition of actin turnover prevented retraction. Results from the present study reveal a new system mediated by kinesin-1 sorting in axons that differentially controls stability of arbor terminals.

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DBZ Regulates Cortical Cell Positioning and Neurite Development by Sustaining the Anterograde Transport of Lis1 and DISC1 through Control of Ndel1 Dual-Phosphorylation

Cited by 21 publications

References 56 publications

Pathogenic POGZ mutation causes impaired cortical development and reversible autism-like phenotypes

Pathogenic POGZ mutation causes impaired cortical development and reversible autism-like phenotypes

Effects of antipsychotic drugs on neurites relevant to schizophrenia treatment

Kinesin-1 sorting in axons controls the differential retraction of arbor terminals

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