c‐Myc controls the fate of neural progenitor cells during cerebral cortex development

2019 ◽  
Vol 235 (4) ◽  
pp. 4011-4021 ◽  
Author(s):  
Xiu‐Li Wang ◽  
Yan‐Xia Ma ◽  
Ren‐Jie Xu ◽  
Jin‐Jin Ma ◽  
Hong‐Cheng Zhang ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Cerebral Cortex Development

scholarly journals Mammalian Fat and Dachsous cadherins regulate apical membrane organization in the embryonic cerebral cortex

2009 ◽  
Vol 185 (6) ◽  
pp. 959-967 ◽  
Author(s):  
Takashi Ishiuchi ◽  
Kazuyo Misaki ◽  
Shigenobu Yonemura ◽  
Masatoshi Takeichi ◽  
Takuji Tanoue
Keyword(s):  
Cerebral Cortex ◽  
Plasma Membrane ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Apical Membrane ◽  
Neural Progenitor ◽  
Apical Plasma Membrane ◽  
Cell Contact ◽  
Membrane Organization ◽  
A Cell

Compartmentalization of the plasma membrane in a cell is fundamental for its proper functions. In this study, we present evidence that mammalian Fat4 and Dachsous1 cadherins regulate the apical plasma membrane organization in the embryonic cerebral cortex. In neural progenitor cells of the cortex, Fat4 and Dachsous1 were concentrated together in a cell–cell contact area positioned more apically than the adherens junction (AJ). These molecules interacted in a heterophilic fashion, affecting their respective protein levels. We further found that Fat4 associated and colocalized with the Pals1 complex. Ultrastructurally, the apical junctions of the progenitor cells comprised the AJ and a stretch of plasma membrane apposition extending apically from the AJ, which positionally corresponded to the Fat4–Dachsous1-positive zone. Depletion of Fat4 or Pals1 abolished this membrane apposition. These results highlight the importance of the Fat4–Dachsous1–Pals1 complex in organizing the apical membrane architecture of neural progenitor cells.

scholarly journals Neural Progenitor Cells in Cerebral Cortex of Epilepsy Patients do not Originate from Astrocytes Expressing GLAST

2016 ◽  
Author(s):  
Meng Chen ◽  
Till B. Puschmann ◽  
Ulrika Wilhelmsson ◽  
Charlotte Örndal ◽  
Marcela Pekna ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Neural Progenitor

scholarly journals Roots of the Malformations of Cortical Development in the Cell Biology of Neural Progenitor Cells

2022 ◽  
Vol 15 ◽  
Author(s):  
Chiara Ossola ◽  
Nereo Kalebic
Keyword(s):  
Cerebral Cortex ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Cortical Development ◽  
Neural Progenitor ◽  
Autism Spectrum ◽  
Model Systems ◽  
Cortical Plate ◽  
Malformations Of Cortical Development ◽  
Brain Functions

The cerebral cortex is a structure that underlies various brain functions, including cognition and language. Mammalian cerebral cortex starts developing during the embryonic period with the neural progenitor cells generating neurons. Newborn neurons migrate along progenitors’ radial processes from the site of their origin in the germinal zones to the cortical plate, where they mature and integrate in the forming circuitry. Cell biological features of neural progenitors, such as the location and timing of their mitoses, together with their characteristic morphologies, can directly or indirectly regulate the abundance and the identity of their neuronal progeny. Alterations in the complex and delicate process of cerebral cortex development can lead to malformations of cortical development (MCDs). They include various structural abnormalities that affect the size, thickness and/or folding pattern of the developing cortex. Their clinical manifestations can entail a neurodevelopmental disorder, such as epilepsy, developmental delay, intellectual disability, or autism spectrum disorder. The recent advancements of molecular and neuroimaging techniques, along with the development of appropriate in vitro and in vivo model systems, have enabled the assessment of the genetic and environmental causes of MCDs. Here we broadly review the cell biological characteristics of neural progenitor cells and focus on those features whose perturbations have been linked to MCDs.

scholarly journals Dual Role of Rbpj in the Maintenance of Neural Progenitor Cells and Neuronal Migration in Cortical Development

2020 ◽  
Vol 30 (12) ◽  
pp. 6444-6457
Author(s):  
Alexander I Son ◽  
Shahid Mohammad ◽  
Toru Sasaki ◽  
Seiji Ishii ◽  
Satoshi Yamashita ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Notch Signaling ◽  
Progenitor Cells ◽  
Knockout Mice ◽  
Neural Progenitor Cells ◽  
Cortical Development ◽  
Neural Progenitor ◽  
Dual Role

Abstract The development of the cerebral cortex is directed by a series of methodically precise events, including progenitor cell proliferation, neural differentiation, and cell positioning. Over the past decade, many studies have demonstrated the critical contributions of Notch signaling in neurogenesis, including that in the developing telencephalon. However, in vivo evidence for the role of Notch signaling in cortical development still remains limited partly due to the redundant functions of four mammalian Notch paralogues and embryonic lethality of the knockout mice. Here, we utilized the conditional deletion and in vivo gene manipulation of Rbpj, a transcription factor that mediates signaling by all four Notch receptors, to overcome these challenges and examined the specific roles of Rbpj in cortical development. We report severe structural abnormalities in the embryonic and postnatal cerebral cortex in Rbpj conditional knockout mice, which provide strong in vivo corroboration of previously reported functions of Notch signaling in neural development. Our results also provide evidence for a novel dual role of Rbpj in cell type-specific regulation of two key developmental events in the cerebral cortex: the maintenance of the undifferentiated state of neural progenitor cells, and the radial and tangential allocation of neurons, possibly through stage-dependent differential regulation of Ngn1.

scholarly journals Neural progenitor cells mediated by H2A.Z.2 regulate microglial development via Cxcl14 in the embryonic brain

2019 ◽  
Vol 116 (48) ◽  
pp. 24122-24132 ◽  
Author(s):  
Zhongqiu Li ◽  
Yanxin Li ◽  
Jianwei Jiao
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Progenitor Cells ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Ventricular Zone ◽  
Neural Progenitor ◽  
The Central Nervous System ◽  
Microglial Development

Microglia, the resident immune cells of the central nervous system, play an important role in the brain. Microglia have a special spatiotemporal distribution during the development of the cerebral cortex. Neural progenitor cells (NPCs) are the main source of neural-specific cells in the early brain. It is unclear whether NPCs affect microglial development and what molecular mechanisms control early microglial localization. H2A.Z.2, a histone variant of H2A, has a key role in gene expression regulation, genomic stability, and chromatin remodeling, but its function in brain development is not fully understood. Here, we found that the specific deletion of H2A.Z.2 in neural progenitor cells led to an abnormal increase in microglia in the ventricular zone/subventricular zone (VZ/SVZ) of the embryonic cortex. Mechanistically, H2A.Z.2 regulated microglial development by incorporating G9a into the promoter region of Cxcl14 and promoted H3k9me2 modification to inhibit the transcription of Cxcl14 in neural progenitor cells. Meanwhile, we found that the deletion of H2A.Z.2 in microglia itself had no significant effect on microglial development in the early cerebral cortex. Our findings demonstrate a key role of H2A.Z.2 in neural progenitor cells in controlling microglial development and broaden our knowledge of 2 different types of cells that may affect each other through crosstalk in the central nervous system.

scholarly journals Zika Virus and Neuropathogenesis: The Unanswered Question of Which Strain Is More Prone to Causing Microcephaly and Other Neurological Defects

2021 ◽  
Vol 15 ◽  
Author(s):  
Emily Louise King ◽  
Nerea Irigoyen
Keyword(s):  
Cerebral Cortex ◽  
Progenitor Cells ◽  
Zika Virus ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
French Polynesia ◽  
Cellular Processes ◽  
Neurotropic Viruses ◽  
Congenital Zika Syndrome ◽  
Induced Apoptosis

Despite being perceived to be a relatively innocuous pathogen during its circulation in Africa in the 20th century, consequent outbreaks in French Polynesia and Latin America revealed the Zika virus (ZIKV) to be capable of causing severe neurological defects. Foetuses infected with the virus during pregnancy developed a range of pathologies including microcephaly, cerebral calcifications and macular scarring. These are now collectively known as Congenital Zika syndrome (CZS). It has been established that the neuropathogenesis of ZIKV results from infection of neural progenitor cells in the developing cerebral cortex. Following this, two main hypotheses have emerged: the virus causes either apoptosis or premature differentiation of neural progenitor cells, reducing the final number of mature neurons in the cerebral cortex. This review describes the cellular processes which could potentially cause virus induced apoptosis or premature differentiation, leading to speculation that a combination of the two may be responsible for the pathologies associated with ZIKV. The review also discusses which specific lineages of the ZIKV can employ these mechanisms. It has been unclear in the past whether the virus evolved its neurotropic capability following circulation in Africa, or if the virus has always caused microcephaly but public health surveillance in Africa had failed to detect it. Understanding the true neuropathogenesis of ZIKV is key to being prepared for further outbreaks in the future, and it will also provide insight into how neurotropic viruses can cause profound and life-long neurological defects.

Sign in / Sign up

Export Citation Format

Share Document