Zbtb16 regulates social cognitive behaviors and neocortical development
Abstract Zinc finger and BTB domain containing 16 (ZBTB16) play the roles in the neural progenitor cell proliferation and neuronal differentiation during development, however, how the function of ZBTB16 is involved in brain function and behaviors unknown. Here we show the deletion of Zbtb16 in mice...
Main Authors: | , , , , , , |
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Format: | Article |
Language: | English |
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Nature Publishing Group
2021-04-01
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Series: | Translational Psychiatry |
Online Access: | https://doi.org/10.1038/s41398-021-01358-y |
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author | Noriyoshi Usui Stefano Berto Ami Konishi Makoto Kondo Genevieve Konopka Hideo Matsuzaki Shoichi Shimada |
author_facet | Noriyoshi Usui Stefano Berto Ami Konishi Makoto Kondo Genevieve Konopka Hideo Matsuzaki Shoichi Shimada |
author_sort | Noriyoshi Usui |
collection | DOAJ |
description | Abstract Zinc finger and BTB domain containing 16 (ZBTB16) play the roles in the neural progenitor cell proliferation and neuronal differentiation during development, however, how the function of ZBTB16 is involved in brain function and behaviors unknown. Here we show the deletion of Zbtb16 in mice leads to social impairment, repetitive behaviors, risk-taking behaviors, and cognitive impairment. To elucidate the mechanism underlying the behavioral phenotypes, we conducted histological analyses and observed impairments in thinning of neocortical layer 6 (L6) and a reduction of TBR1+ neurons in Zbtb16 KO mice. Furthermore, we found increased dendritic spines and microglia, as well as developmental defects in oligodendrocytes and neocortical myelination in the prefrontal cortex (PFC) of Zbtb16 KO mice. Using genomics approaches, we identified the Zbtb16 transcriptome that includes genes involved in neocortical maturation such as neurogenesis and myelination, and both autism spectrum disorder (ASD) and schizophrenia (SCZ) pathobiology. Co-expression networks further identified Zbtb16-correlated modules that are unique to ASD or SCZ, respectively. Our study provides insight into the novel roles of ZBTB16 in behaviors and neocortical development related to the disorders. |
first_indexed | 2024-12-17T00:53:41Z |
format | Article |
id | doaj.art-e3e5f052aa054a5e8ea706dc84db2397 |
institution | Directory Open Access Journal |
issn | 2158-3188 |
language | English |
last_indexed | 2024-12-17T00:53:41Z |
publishDate | 2021-04-01 |
publisher | Nature Publishing Group |
record_format | Article |
series | Translational Psychiatry |
spelling | doaj.art-e3e5f052aa054a5e8ea706dc84db23972022-12-21T22:09:42ZengNature Publishing GroupTranslational Psychiatry2158-31882021-04-0111111510.1038/s41398-021-01358-yZbtb16 regulates social cognitive behaviors and neocortical developmentNoriyoshi Usui0Stefano Berto1Ami Konishi2Makoto Kondo3Genevieve Konopka4Hideo Matsuzaki5Shoichi Shimada6Department of Neuroscience and Cell Biology, Graduate School of Medicine, Osaka UniversityDepartment of Neuroscience, University of Texas Southwestern Medical CenterDepartment of Neuroscience and Cell Biology, Graduate School of Medicine, Osaka UniversityDepartment of Neuroscience and Cell Biology, Graduate School of Medicine, Osaka UniversityDepartment of Neuroscience, University of Texas Southwestern Medical CenterDepartment of Child Development, United Graduate School of Child Development, Osaka UniversityDepartment of Neuroscience and Cell Biology, Graduate School of Medicine, Osaka UniversityAbstract Zinc finger and BTB domain containing 16 (ZBTB16) play the roles in the neural progenitor cell proliferation and neuronal differentiation during development, however, how the function of ZBTB16 is involved in brain function and behaviors unknown. Here we show the deletion of Zbtb16 in mice leads to social impairment, repetitive behaviors, risk-taking behaviors, and cognitive impairment. To elucidate the mechanism underlying the behavioral phenotypes, we conducted histological analyses and observed impairments in thinning of neocortical layer 6 (L6) and a reduction of TBR1+ neurons in Zbtb16 KO mice. Furthermore, we found increased dendritic spines and microglia, as well as developmental defects in oligodendrocytes and neocortical myelination in the prefrontal cortex (PFC) of Zbtb16 KO mice. Using genomics approaches, we identified the Zbtb16 transcriptome that includes genes involved in neocortical maturation such as neurogenesis and myelination, and both autism spectrum disorder (ASD) and schizophrenia (SCZ) pathobiology. Co-expression networks further identified Zbtb16-correlated modules that are unique to ASD or SCZ, respectively. Our study provides insight into the novel roles of ZBTB16 in behaviors and neocortical development related to the disorders.https://doi.org/10.1038/s41398-021-01358-y |
spellingShingle | Noriyoshi Usui Stefano Berto Ami Konishi Makoto Kondo Genevieve Konopka Hideo Matsuzaki Shoichi Shimada Zbtb16 regulates social cognitive behaviors and neocortical development Translational Psychiatry |
title | Zbtb16 regulates social cognitive behaviors and neocortical development |
title_full | Zbtb16 regulates social cognitive behaviors and neocortical development |
title_fullStr | Zbtb16 regulates social cognitive behaviors and neocortical development |
title_full_unstemmed | Zbtb16 regulates social cognitive behaviors and neocortical development |
title_short | Zbtb16 regulates social cognitive behaviors and neocortical development |
title_sort | zbtb16 regulates social cognitive behaviors and neocortical development |
url | https://doi.org/10.1038/s41398-021-01358-y |
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