Medaka and zebrafish contactin1 mutants as a model for understanding neural circuits for motor coordination

Takeuchi, Miki; Inoue, Chikako; Goshima, Akiko; Nagao, Yusuke; Shimizu, Koichi; Miyamoto, Hiroki; Shimizu, Takashi; Hashimoto, Hisashi; Yonemura, Shigenobu; Kawahara, Atsuo; Hirata, Yutaka; Yoshida, Masayuki; Hibi, Masahiko

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Medaka and zebrafish contactin1 mutants as a model for understanding neural circuits for motor coordination

http://hdl.handle.net/2237/27156

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Item type

学術雑誌論文 / Journal Article(1)

公開日

2017-12-08

タイトル

Medaka and zebrafish contactin1 mutants as a model for understanding neural circuits for motor coordination

著者

権利

権利情報

"This is the peer reviewed version of the following article: [Takeuchi, M., Inoue, C., Goshima, A., Nagao, Y., Shimizu, K., Miyamoto, H., Shimizu, T., Hashimoto, H., Yonemura, S., Kawahara, A., Hirata, Y., Yoshida, M. and Hibi, M. (2017), Medaka and zebrafish contactin1 mutants as a model for understanding neural circuits for motor coordination. Genes Cells, 22: 723–741. doi:10.1111/gtc.12509], which has been published in final form at [http://doi.org/10.1111/gtc.12509]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving."

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Abstract

内容記述

A spontaneous medaka ro mutant shows abnormal wobbling and rolling swimming behaviors. By positional cloning, we mapped the ro locus to a region containing the gene encoding Contactin1b (Cntn1b), which is an immunoglobulin (Ig)-superfamily domain-containing membrane-anchored protein. The ro mutant had a deletion in the cntn1b gene that introduced a premature stop codon. Furthermore, cntn1b mutants generated by the CRISPR/Cas9 system and trans-heterozygotes of the CRISPR mutant allele and ro had abnormal swimming behavior, indicating that the cntn1b gene was responsible for the ro-mutant phenotype. We also established zebrafish cntn1a and cntn1b mutants by transcription activator-like effector nucleases (TALENs). Zebrafish cntn1b but not cntn1a mutants showed abnormal swimming behaviors similar to those in the ro mutant, suggesting that Cntn1b plays a conserved role in the formation or function of the neural circuits that control swimming in teleosts. Although Cntn1-deficient mice have abnormal cerebellar neural circuitry, there was no apparent histological abnormality in the cerebellum of medaka or zebrafish cntn1b mutants. The medaka cntn1b mutants had defective optokinetic response (OKR) adaptation and abnormal rheotaxis (body positioning relative to water flow). Medaka and zebrafish cntn1b mutants are effective models for studying the neural circuits involved in motor learning and motor coordination.

出版者

Wiley

言語

eng

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資源

http://purl.org/coar/resource_type/c_6501

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journal article

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ISSN

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1356-9597

書誌情報

GENES TO CELLS

巻 22, 号 8, p. 723-741, 発行日 2017-08

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author

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http://doi.org/10.1111/gtc.12509

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DOI

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識別子

http://hdl.handle.net/2237/27156

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HDL

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Medaka and zebrafish contactin1 mutants as a model for understanding neural circuits for motor coordination

× Takeuchi, Miki

× Inoue, Chikako

× Goshima, Akiko

× Nagao, Yusuke

× Shimizu, Koichi

× Miyamoto, Hiroki

× Shimizu, Takashi

× Hashimoto, Hisashi

× Yonemura, Shigenobu

× Kawahara, Atsuo

× Hirata, Yutaka

× Yoshida, Masayuki

× Hibi, Masahiko

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