{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T23:38:49Z","timestamp":1790206729683,"version":"4.1.0"},"reference-count":70,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2017,6,22]],"date-time":"2017-06-22T00:00:00Z","timestamp":1498089600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes to Cells"],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:p>A spontaneous medaka <jats:italic>ro<\/jats:italic> mutant shows abnormal wobbling and rolling swimming behaviors. By positional cloning, we mapped the <jats:italic>ro<\/jats:italic> locus to a region containing the gene encoding Contactin1b (Cntn1b), which is an immunoglobulin (Ig)\u2010superfamily domain\u2010containing membrane\u2010anchored protein. The <jats:italic>ro<\/jats:italic> mutant had a deletion in the <jats:italic>cntn1b<\/jats:italic> gene that introduced a premature stop codon. Furthermore, <jats:italic>cntn1b<\/jats:italic> mutants generated by the <jats:styled-content style=\"fixed-case\">CRISPR<\/jats:styled-content>\/Cas9 system and trans\u2010heterozygotes of the <jats:styled-content style=\"fixed-case\">CRISPR<\/jats:styled-content> mutant allele and <jats:italic>ro<\/jats:italic> had abnormal swimming behavior, indicating that the <jats:italic>cntn1b<\/jats:italic> gene was responsible for the <jats:italic>ro\u2010<\/jats:italic>mutant phenotype. We also established zebrafish <jats:italic>cntn1a<\/jats:italic> and <jats:italic>cntn1b<\/jats:italic> mutants by transcription activator\u2010like effector nucleases (<jats:styled-content style=\"fixed-case\">TALEN<\/jats:styled-content>s). Zebrafish <jats:italic>cntn1b<\/jats:italic> but not <jats:italic>cntn1a<\/jats:italic> mutants showed abnormal swimming behaviors similar to those in the <jats:italic>ro<\/jats:italic> mutant, suggesting that Cntn1b plays a conserved role in the formation or function of the neural circuits that control swimming in teleosts. Although <jats:italic>Cntn1<\/jats:italic>\u2010deficient mice have abnormal cerebellar neural circuitry, there was no apparent histological abnormality in the cerebellum of medaka or zebrafish <jats:italic>cntn1b<\/jats:italic> mutants. The medaka <jats:italic>cntn1b<\/jats:italic> mutants had defective optokinetic response (<jats:styled-content style=\"fixed-case\">OKR<\/jats:styled-content>) adaptation and abnormal rheotaxis (body positioning relative to water flow). Medaka and zebrafish <jats:italic>cntn1b<\/jats:italic> mutants are effective models for studying the neural circuits involved in motor learning and motor coordination.<\/jats:p>","DOI":"10.1111\/gtc.12509","type":"journal-article","created":{"date-parts":[[2017,6,22]],"date-time":"2017-06-22T07:58:38Z","timestamp":1498118318000},"page":"723-741","source":"Crossref","is-referenced-by-count":14,"title":["Medaka and zebrafish <i>contactin1<\/i> mutants as a model for understanding neural circuits for motor coordination"],"prefix":"10.1111","volume":"22","author":[{"given":"Miki","family":"Takeuchi","sequence":"first","affiliation":[{"name":"Laboratory of Organogenesis and Organ Function Bioscience and Biotechnology Center Nagoya University Furo Chikusa Nagoya Aichi 464\u20108601 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chikako","family":"Inoue","sequence":"additional","affiliation":[{"name":"Laboratory of Organogenesis and Organ Function Bioscience and 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