scholarly journals Morphology and Mechanics of Daughter Cells "Delaminating" from the Ventricular Zone of the Developing Neocortex

2007 ◽  
Vol 1 (2) ◽  
pp. 99-101 ◽  
Author(s):  
Takai Miyata
Keyword(s):  
Ventricular Zone ◽  
Daughter Cells ◽  
Developing Neocortex

Differential expression of mammalian Numb, Numblike and Notch1 suggests distinct roles during mouse cortical neurogenesis

Development ◽  
1997 ◽  
Vol 124 (10) ◽  
pp. 1887-1897 ◽  
Author(s):  
W. Zhong ◽  
M.M. Jiang ◽  
G. Weinmaster ◽  
L.Y. Jan ◽  
Y.N. Jan
Keyword(s):  
Sequence Similarity ◽  
Ventricular Zone ◽  
Cell Interaction ◽  
Cortical Plate ◽  
Loss Of Function ◽  
Cortical Neurogenesis ◽  
Daughter Cells ◽  
Embryonic Nervous System ◽  
Progenitor Cell Proliferation ◽  
Developing Neocortex

During Drosophila neurogenesis, asymmetric cell divisions are achieved by differential segregation of Numb (d-Numb) into one of the daughter cells to cause a bias in the Notch mediated cell-cell interaction. We have isolated a second mammalian gene with significant sequence similarity to d-numb, mouse numblike. When expressed in dividing neural precursors in Drosophila, Numblike is symmetrically distributed in the cytoplasm, unlike endogenous d-Numb or expressed mouse Numb (m-Numb), both of which are asymmetrically localized to one half of the cell membrane. In d-numb loss-of-function mutant embryos, expression of Numblike allows both daughter cells of a neural precursor to adopt the fate of the cell that normally inherits d-Numb. In mice, numblike mRNA is preferentially expressed in adult and embryonic nervous system. In the developing neocortex, Numblike is expressed in postmitotic neurons in the cortical plate, but not in progenitors within the ventricular zone where m-Numb and Notch1 are expressed. We have also found that, in dividing cortical progenitors, Notch1 is distributed around the entire membrane, unlike m-Numb which is asymmetrically localized to the apical membrane. We propose that an interplay between cell-intrinsic mechanisms (executed by m-numb and numblike) and cell-extrinsic mechanisms (mediated by Notch1) may be involved in both progenitor cell proliferation and neuronal differentiation during mammalian cortical neurogenesis.

scholarly journals Targeted Ablation and Reorganization of the Principal Preplate Neurons and Their Neuroblasts Identified by Golli Promoter Transgene Expression in the Neocortex of Mice

ASN NEURO ◽  
2009 ◽  
Vol 1 (4) ◽  
pp. AN20090038 ◽  
Author(s):  
Yuan-Yun Xie ◽  
Erin Jacobs ◽  
Robin Fisher
Keyword(s):  
Fluorescent Protein ◽  
Ventricular Zone ◽  
Vertical Gradient ◽  
Prenatal Development ◽  
Specific Cell ◽  
Genetic Ablation ◽  
Developing Neocortex ◽  
Total Complement ◽  
Green Fluorescent ◽  
Simplex Virus

The present study delineates the cellular responses of dorsal pallium to targeted genetic ablation of the principal preplate neurons of the neocortex. Ganciclovir treatment during prenatal development (E11-E13; where E is embryonic day) of mice selectively killed cells with shared S-phase vulnerability and targeted expression of a GPT [golli promoter transgene, linked to HSV-TK (herpes simplex virus-thymidine kinase), τ-eGFP (τ-enhanced green fluorescent protein) and lacZ (lacZ galactosidase) reporters] localized in preplate neurons. Morphogenetic fates of attacked neurons and neuroblasts, and their successors, were assessed by multiple labelling in time-series comparisons between ablated (HSV-TK+/0) and control (HSV-TK0/0) littermates. During ablation generation, neocortical growth was suppressed, and compensatory reorganization of non-GPT ventricular zone progenitors of dorsal pallium produced replacements for killed GPT neuroblasts. Replacement and surviving GPT neuroblasts then produced replacements for killed GPT neurons. Near-normal restoration of their complement delayed the settlement of GPT neurons into the reconstituted preplate, which curtailed the outgrowth of pioneer corticofugal axons. Based on this evidence, we conclude that specific cell killing in ablated mice can eliminate a major fraction of GPT neurons, with insignificant bystander killing. Also, replacement GPT neurons in ablated mice originate exclusively by proliferation from intermediate progenitor GPT neuroblasts, whose complement is maintained by non-GPT progenitors for inductive regulation of the total complement of GPT neurons. Finally, GPT neurons in both normal and ablated mice meet all morphogenetic criteria, including the ‘outside-in’ vertical gradient of settlement, presently used to identify principal preplate neurons. In ablated mice, delayed organization of these neurons desynchronizes and isolates developing neocortex from the rest of the brain, and permanently impairs its connectivity.

scholarly journals Phosphorylation of Focal Adhesion Kinase at Tyr925: Role in Glia-Dependent and Independent Migration Through Regulating Cofilin and N-Cadherin

2021 ◽  
Author(s):  
Lingzhen Song ◽  
Shanting Zhao ◽  
Michael Frotscher ◽  
Xuejun Chai
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Neuronal Migration ◽  
Cortical Neurons ◽  
Molecular Mechanisms ◽  
Ventricular Zone ◽  
Focal Adhesions ◽  
Developing Neocortex ◽  
Reelin Signaling ◽  
Highly Correlated

Abstract The adult neocortex is a six-layered structure, consisting of nearly continuous layers of neurons that are generated with large temporal diversity. During development, cortical neurons originating from the ventricular zone migrate towards the Reelin-containing marginal zone in an inside-out arrangement. Focal adhesion kinase (FAK), one tyrosine kinase localizing to focal adhesions, has been shown to be activated by Src, an important downstream molecule of Reelin signaling, at tyrosine 925 (Y925). Up to date, the precise molecular mechanisms of FAK and its phosphorylation at Y925 during neuronal migration are still unclear. Combining in utero electroporation with immunohistochemistry and live imaging, we examined the function of FAK in regulating neuronal migration. We show that phosphorylated FAK is colocalized with Reelin positive cells in the developing neocortex and hippocampus. Phosphorylation of FAK at Y925 is significantly reduced in reeler mice. Overexpression and dephosphorylation of FAK impair locomotion and translocation, resulting in migration inhibition and dislocation of both late-born and early-born neurons. These migration defects are highly correlated to the function of FAK in regulating cofilin phosphorylation and N-Cadherin expression, both are involved in Reelin signaling pathway. Thus, phosphorylation of focal adhesion kinase at Y925 is crucial for both glia-dependent and independent neuronal migration.

scholarly journals Cell Coupling and Uncoupling in the Ventricular Zone of Developing Neocortex

1997 ◽  
Vol 17 (18) ◽  
pp. 7037-7044 ◽  
Author(s):  
Kevin Bittman ◽  
David F. Owens ◽  
Arnold R. Kriegstein ◽  
Joseph J. LoTurco
Keyword(s):  
Ventricular Zone ◽  
Cell Coupling ◽  
Developing Neocortex

scholarly journals Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex

Science ◽  
2019 ◽  
Vol 364 (6440) ◽  
pp. eaav2522 ◽  
Author(s):  
L. Telley ◽  
G. Agirman ◽  
J. Prados ◽  
N. Amberg ◽  
S. Fièvre ◽  
...  
Keyword(s):  
Ventricular Zone ◽  
Mouse Embryos ◽  
High Temporal Resolution ◽  
Neuronal Diversity ◽  
Core Set ◽  
Evolutionarily Conserved ◽  
Repressor Complex ◽  
Age Dependent ◽  
Developing Neocortex ◽  
Successive Generations

During corticogenesis, distinct subtypes of neurons are sequentially born from ventricular zone progenitors. How these cells are molecularly temporally patterned is poorly understood. We used single-cell RNA sequencing at high temporal resolution to trace the lineage of the molecular identities of successive generations of apical progenitors (APs) and their daughter neurons in mouse embryos. We identified a core set of evolutionarily conserved, temporally patterned genes that drive APs from internally driven to more exteroceptive states. We found that the Polycomb repressor complex 2 (PRC2) epigenetically regulates AP temporal progression. Embryonic age–dependent AP molecular states are transmitted to their progeny as successive ground states, onto which essentially conserved early postmitotic differentiation programs are applied, and are complemented by later-occurring environment-dependent signals. Thus, epigenetically regulated temporal molecular birthmarks present in progenitors act in their postmitotic progeny to seed adult neuronal diversity.

Stimulated Virus Production in Vinblastine and Cytochalasin-Induced Multinucleate Cells

1970 ◽  
Vol 28 ◽  
pp. 186-187
Author(s):  
Krishan Awtar
Keyword(s):  
Cell Division ◽  
Normal Cell ◽  
Virus Production ◽  
Multinucleate Cells ◽  
Daughter Cells ◽  
Cell Divisions ◽  
Nuclear Membranes ◽  
Division 2 ◽  
Vinblastine Sulfate

Exposure of cells to low sublethal but mitosis-arresting doses of vinblastine sulfate (Velban) results in the initial arrest of cells in mitosis followed by their subsequent return to an “interphase“-like stage. A large number of these cells reform their nuclear membranes and form large multimicronucleated cells, some containing as many as 25 or more micronuclei (1). Formation of large multinucleate cells is also caused by cytochalasin, by causing the fusion of daughter cells at the end of an otherwise .normal cell division (2). By the repetition of this process through subsequent cell divisions, large cells with 6 or more nuclei are formed.

Fine Structure of Cytochalasin Induced Polyploid Cells

1968 ◽  
Vol 26 ◽  
pp. 122-123
Author(s):  
Awtar Krishan ◽  
Nestor Bohonos
Keyword(s):  
Fine Structure ◽  
Cytochalasin B ◽  
Present Report ◽  
Cell Monolayer ◽  
Polyploid Cell ◽  
Specific Cell ◽  
Nuclear Surface ◽  
Unsuccessful Attempt ◽  
Daughter Cells ◽  
Polyploid Cells

Cytochalasin B, a mould metabolite from Helminthosporium dermatioideum has been shown to interfere with specific cell activities such as cytoplasmic cleavage and cell movement. Cells undergoing nuclear division in the presence of cytochalasin B are unable to complete the separation of the resulting daughter cells. In time-lapse studies, the daughter cells coalesce after an initial unsuccessful attempt at separation and form large multinucleate polyploid cells. The present report describes the fine structure of the large polyploid cells induced in Earle's L-cell monolayer cultures by exposure to cytochalasin B (lγ/ml) for 92 hours.In the present material we have seen as many as 7 nuclei in these polyploid cells. Treatment with cytochalasin B for longer periods of time (6 to 7 days, with one medium change on the 3rd day) did not increase the number of nuclei beyond the 7 nuclei stage. Figure 1 shows a large polyploid cell with four nuclei. These nuclei are indistinguishable in their fine structure from those of the cells from control cultures but often show unusually large numbers of cytoplasmic invaginations and extensions of the nuclear surface (Figure 2).

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