title: CDYL Deficiency Disrupts Neuronal Migration and Increases Susceptibility to Epilepsy.
abstract: During brain development, the correct migration of newborn neurons is one of the determinants of circuit formation, and neuronal migration defects may lead to neurological and psychiatric disorders. The molecular mechanisms underlying neuronal migration and related disorders are poorly understood. Here, we report that Chromodomain Y-like (CDYL) is critical for neuronal migration in mice. Knocking down CDYL caused neuronal migration defects and disrupted both mobility and multipolar-to-bipolar transition of migrating neurons. We find that CDYL regulates neuronal migration by transcriptionally repressing RhoA. In addition, CDYL deficiency increased the excitability of cortical pyramidal neurons and the susceptibility of mice to convulsant-induced seizures. These results demonstrate that CDYL is a regulator of neuronal migration and shed light on the pathogenesis of seizure-related neurodevelopmental disorders.
authors.affiliation: Neuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Key Laboratory for Neuroscience, Ministry of Education/National Health and Family Planning Commission, Peking University, Beijing 100191, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Qin
authors.affiliation: Neuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Key Laboratory for Neuroscience, Ministry of Education/National Health and Family Planning Commission, Peking University, Beijing 100191, China.
authors.forename: Shuai
authors.initials: S
authors.lastname: Cao
authors.affiliation: Neuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Key Laboratory for Neuroscience, Ministry of Education/National Health and Family Planning Commission, Peking University, Beijing 100191, China.
authors.forename: Tianjie
authors.initials: T
authors.lastname: Lyu
authors.affiliation: Neuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Key Laboratory for Neuroscience, Ministry of Education/National Health and Family Planning Commission, Peking University, Beijing 100191, China.
authors.forename: Cai
authors.initials: C
authors.lastname: Qi
authors.affiliation: Department of Anatomy, Histology and Embryology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
authors.forename: Weiguang
authors.initials: W
authors.lastname: Zhang
authors.affiliation: Neuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Key Laboratory for Neuroscience, Ministry of Education/National Health and Family Planning Commission, Peking University, Beijing 100191, China; PKU-IDG/McGovern Institute for Brain Research, Peking University, Beijing 100871, China. Electronic address: wangy66@bjmu.edu.cn.
authors.forename: Yun
authors.initials: Y
authors.lastname: Wang
mesh_terms: D008841:Actin Cytoskeleton / Q000378:metabolism; D000199:Actins / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000473:pathology; D002465:Cell Movement; D016764:Cell Polarity; D002843:Chromatin / Q000378:metabolism; D056970:Co-Repressor Proteins / Q000378:metabolism; D004198:Disease Susceptibility; D004827:Epilepsy / Q000378:metabolism* / Q000473:pathology*; D055785:Gene Knockdown Techniques; D051548:Histone Acetyltransferases / Q000172:deficiency* / Q000378:metabolism; D006657:Histones / Q000378:metabolism; D006836:Hydro-Lyases; D008297:Male; D008810:Mice, Inbred C57BL; D008813:Mice, Inbred ICR; D009474:Neurons / Q000378:metabolism* / Q000473:pathology*; D010433:Pentylenetetrazole; D058105:Polymerization; D015398:Signal Transduction; D020742:rhoA GTP-Binding Protein / Q000378:metabolism
chemical_list: D000199:Actins; D002843:Chromatin; D056970:Co-Repressor Proteins; D006657:Histones; D051548:Histone Acetyltransferases; D020742:rhoA GTP-Binding Protein; C485563:Cdyl protein, mouse; D006836:Hydro-Lyases; D010433:Pentylenetetrazole
keywords: CDYL; RhoA; epilepsy; neuronal migration; transcription