During brain development, the proliferation and differentiation of neural stem cells (NSCs) are precisely regulated. Defects in embryonic brain development can lead to serious developmental disorders. The cerebral cortex is the most evolved and complicated structure in the mammalian brain. The process of neuronal production, also known as neurogenesis, plays crucial roles in cerebral development and can affect the function of the neocortex. Ccdc25 is a newly discovered molecule. It has been proved that it can play an important role in tumor. However, its function in neural systems is unclear. In this study, we find that in early embryonic development, Ccdc25 can express in the brain. Suppression of the Ccdc25 mediated by shRNAs causes the increase of the Ki67- or BrdU-positive NSCs proliferation and inhibits the premature terminal mitosis and neuronal differentiation. Simultaneously, overexpression of Ccdc2525 inhibits the proliferation and promotes the differentiation of NSCs. Knockdown of Ccdc25 also affects neuronal maturation, the number of branches of neurons cultured in vitro decreased, and the number of axons became shorter. We also examined the expression profile of NSCs when Ccdc25 was knocked down by RNA sequencing technique. We found that Ccdc25 regulates the development of NSCs through Egr1. Egr1 knockdown can result in a phenotype similar to Ccdc25, while the overexpression of Egr1 can also rescue the phenotype of Ccdc25 knockdown. In conclusion, Ccdc25 can affect the proliferation and differentiation of NSCs and the maturation of neuron.
{"title":"Ccdc25 regulates neurogenesis during the brain development","authors":"Chong Wang, Jie Qin, Jianwei Jiao, Fen Ji","doi":"10.1002/dneu.22911","DOIUrl":"10.1002/dneu.22911","url":null,"abstract":"<p>During brain development, the proliferation and differentiation of neural stem cells (NSCs) are precisely regulated. Defects in embryonic brain development can lead to serious developmental disorders. The cerebral cortex is the most evolved and complicated structure in the mammalian brain. The process of neuronal production, also known as neurogenesis, plays crucial roles in cerebral development and can affect the function of the neocortex. Ccdc25 is a newly discovered molecule. It has been proved that it can play an important role in tumor. However, its function in neural systems is unclear. In this study, we find that in early embryonic development, Ccdc25 can express in the brain. Suppression of the Ccdc25 mediated by shRNAs causes the increase of the Ki67- or BrdU-positive NSCs proliferation and inhibits the premature terminal mitosis and neuronal differentiation. Simultaneously, overexpression of Ccdc2525 inhibits the proliferation and promotes the differentiation of NSCs. Knockdown of Ccdc25 also affects neuronal maturation, the number of branches of neurons cultured in vitro decreased, and the number of axons became shorter. We also examined the expression profile of NSCs when Ccdc25 was knocked down by RNA sequencing technique. We found that Ccdc25 regulates the development of NSCs through Egr1. Egr1 knockdown can result in a phenotype similar to Ccdc25, while the overexpression of Egr1 can also rescue the phenotype of Ccdc25 knockdown. In conclusion, Ccdc25 can affect the proliferation and differentiation of NSCs and the maturation of neuron.</p>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9627822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Timothy R. Young, Dylan Black, Hannan Mansuri, Toshitaka Oohashi, Xiao-Hong Zhou, Atomu Sawatari, Catherine A. Leamey
The patterning of binocular vision requires distinct molecular pathways for inputs arising from each side of the nervous system. Recent studies have demonstrated important roles for members of the Ten-m/Odz/teneurin family in the development of ipsilateral retinal projections. Here, we further highlight the significance of this gene family in visual development by identifying a role for Ten-m4 during the formation of the ipsilateral projection in the mouse. Ten-m4 was found to be expressed in the retina, dorsal lateral geniculate nucleus (dLGN), superior colliculus (SC), and primary visual cortex (V1) during development. Anterograde and retrograde tracing experiments in Ten-m4 knockout (KO) mice revealed a specific increase in ipsilateral retinal ganglion cells projecting to dLGN and SC. This increase was most prominent in regions corresponding to temporal retina. Consistent with this, EphB1 expression in the retina around the time of decussation was enhanced in this temporal region for KO mice, suggesting that the increased size of the ipsilateral population arises due to an increased number of retinal ganglion cells remaining ipsilaterally at the optic chiasm due to EphB1-mediated repulsion. The ectopic ipsilaterally targeted retinal ganglion cell projection observed in Ten-m4 KOs was associated with changes in response to ethologically relevant visual stimuli. Together, these data demonstrate a requirement for Ten-m4 in the establishment of ipsilateral projections from the retina, which likely acts in combination with other Ten-m members (Ten-m2 and Ten-m3) to promote the formation of functional binocular circuits.
{"title":"Ten-m4 plays a unique role in the establishment of binocular visual circuits","authors":"Timothy R. Young, Dylan Black, Hannan Mansuri, Toshitaka Oohashi, Xiao-Hong Zhou, Atomu Sawatari, Catherine A. Leamey","doi":"10.1002/dneu.22912","DOIUrl":"10.1002/dneu.22912","url":null,"abstract":"<p>The patterning of binocular vision requires distinct molecular pathways for inputs arising from each side of the nervous system. Recent studies have demonstrated important roles for members of the Ten-m/Odz/teneurin family in the development of ipsilateral retinal projections. Here, we further highlight the significance of this gene family in visual development by identifying a role for Ten-m4 during the formation of the ipsilateral projection in the mouse. Ten-m4 was found to be expressed in the retina, dorsal lateral geniculate nucleus (dLGN), superior colliculus (SC), and primary visual cortex (V1) during development. Anterograde and retrograde tracing experiments in Ten-m4 knockout (KO) mice revealed a specific increase in ipsilateral retinal ganglion cells projecting to dLGN and SC. This increase was most prominent in regions corresponding to temporal retina. Consistent with this, EphB1 expression in the retina around the time of decussation was enhanced in this temporal region for KO mice, suggesting that the increased size of the ipsilateral population arises due to an increased number of retinal ganglion cells remaining ipsilaterally at the optic chiasm due to EphB1-mediated repulsion. The ectopic ipsilaterally targeted retinal ganglion cell projection observed in Ten-m4 KOs was associated with changes in response to ethologically relevant visual stimuli. Together, these data demonstrate a requirement for Ten-m4 in the establishment of ipsilateral projections from the retina, which likely acts in combination with other Ten-m members (Ten-m2 and Ten-m3) to promote the formation of functional binocular circuits.</p>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dneu.22912","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9627827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}