The actin‐cytoskeleton associating protein BASP1 regulates neural progenitor localization in the neural tube

Neural Progenitor Cells Undergoing Yap/Tead-Mediated Enhanced Self-Renewal Form Heterotopias More Easily in the Diencephalon than in the Telencephalon

Neurochemical Research ◽

10.1007/s11064-017-2390-x ◽

2018 ◽

Vol 43 (1) ◽

pp. 180-189 ◽

Cited By ~ 10

Author(s):

Kanako Saito ◽

Ryotaro Kawasoe ◽

Hiroshi Sasaki ◽

Ayano Kawaguchi ◽

Takaki Miyata

Keyword(s):

Progenitor Cells ◽

Neural Tube ◽

Neural Progenitor Cells ◽

Three Dimensional ◽

Neural Progenitor ◽

Hippo Signaling ◽

Apical Surface ◽

Elevated Expression ◽

Underlying Mechanisms ◽

The Brain

Abstract Spatiotemporally ordered production of cells is essential for brain development. Normally, most undifferentiated neural progenitor cells (NPCs) face the apical (ventricular) surface of embryonic brain walls. Pathological detachment of NPCs from the apical surface and their invasion of outer neuronal territories, i.e., formation of NPC heterotopias, can disrupt the overall structure of the brain. Although NPC heterotopias have previously been observed in a variety of experimental contexts, the underlying mechanisms remain largely unknown. Yes-associated protein 1 (Yap1) and the TEA domain (Tead) proteins, which act downstream of Hippo signaling, enhance the stem-like characteristics of NPCs. Elevated expression of Yap1 or Tead in the neural tube (future spinal cord) induces massive NPC heterotopias, but Yap/Tead-induced expansion of NPCs in the developing brain has not been previously reported to produce NPC heterotopias. To determine whether NPC heterotopias occur in a regionally characteristic manner, we introduced the Yap1-S112A or Tead-VP16 into NPCs of the telencephalon and diencephalon, two neighboring but distinct forebrain regions, of embryonic day 10 mice by in utero electroporation, and compared NPC heterotopia formation. Although NPCs in both regions exhibited enhanced stem-like behaviors, heterotopias were larger and more frequent in the diencephalon than in the telencephalon. This result, the first example of Yap/Tead-induced NPC heterotopia in the forebrain, reveals that Yap/Tead-induced NPC heterotopia is not specific to the neural tube, and also suggests that this phenomenon depends on regional factors such as the three-dimensional geometry and assembly of these cells.

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N-cadherin–mediated cell adhesion restricts cell proliferation in the dorsal neural tube

Molecular Biology of the Cell ◽

10.1091/mbc.e10-08-0675 ◽

2011 ◽

Vol 22 (9) ◽

pp. 1505-1515 ◽

Cited By ~ 18

Author(s):

Kavita Chalasani ◽

Rachel M. Brewster

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Neural Tube ◽

Neural Progenitor ◽

Neural Progenitors ◽

Cell Cycle Exit ◽

Dorsal Neural Tube ◽

Binding Partners ◽

Hh Signaling ◽

Cell Cycle Length

Neural progenitors are organized as a pseudostratified epithelium held together by adherens junctions (AJs), multiprotein complexes composed of cadherins and α- and β-catenin. Catenins are known to control neural progenitor division; however, it is not known whether they function in this capacity as cadherin binding partners, as there is little evidence that cadherins themselves regulate neural proliferation. We show here that zebrafish N-cadherin (N-cad) restricts cell proliferation in the dorsal region of the neural tube by regulating cell-cycle length. We further reveal that N-cad couples cell-cycle exit and differentiation, as a fraction of neurons are mitotic in N-cad mutants. Enhanced proliferation in N-cad mutants is mediated by ligand-independent activation of Hedgehog (Hh) signaling, possibly caused by defective ciliogenesis. Furthermore, depletion of Hh signaling results in the loss of junctional markers. We therefore propose that N-cad restricts the response of dorsal neural progenitors to Hh and that Hh signaling limits the range of its own activity by promoting AJ assembly. Taken together, these observations emphasize a key role for N-cad–mediated adhesion in controlling neural progenitor proliferation. In addition, these findings are the first to demonstrate a requirement for cadherins in synchronizing cell-cycle exit and differentiation and a reciprocal interaction between AJs and Hh signaling.

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Neural tube defects and impaired neural progenitor cell proliferation in Gβ1-deficient mice

Developmental Dynamics ◽

10.1002/dvdy.22256 ◽

2010 ◽

Vol 239 (4) ◽

pp. 1089-1101 ◽

Cited By ~ 45

Author(s):

Hiroaki Okae ◽

Yoichiro Iwakura

Keyword(s):

Cell Proliferation ◽

Neural Tube ◽

Neural Tube Defects ◽

Progenitor Cell ◽

Neural Progenitor Cell ◽

Neural Progenitor ◽

Progenitor Cell Proliferation ◽

Deficient Mice

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Fat1 interacts with Fat4 to regulate neural tube closure, neural progenitor proliferation and apical constriction during mouse brain development

Development ◽

10.1242/dev.123539 ◽

2015 ◽

Vol 142 (16) ◽

pp. 2781-2791 ◽

Cited By ~ 30

Author(s):

C. Badouel ◽

M. A. Zander ◽

N. Liscio ◽

M. Bagherie-Lachidan ◽

R. Sopko ◽

...

Keyword(s):

Brain Development ◽

Mouse Brain ◽

Neural Tube ◽

Neural Progenitor ◽

Neural Tube Closure ◽

Apical Constriction ◽

Tube Closure ◽

Mouse Brain Development

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EZH2 regulates neuroepithelium structure and neuroblast proliferation by repressing p21

Open Biology ◽

10.1098/rsob.150227 ◽

2016 ◽

Vol 6 (4) ◽

pp. 150227 ◽

Cited By ~ 14

Author(s):

Naiara Akizu ◽

María Alejandra García ◽

Conchi Estarás ◽

Raquel Fueyo ◽

Carmen Badosa ◽

...

Keyword(s):

Chick Embryo ◽

Neural Tube ◽

Transcriptional Profiling ◽

Neural Progenitor ◽

Vertebrate Development ◽

Structural Alterations ◽

Neural Tubes ◽

Functional Assays ◽

Neuroblast Proliferation

The function of EZH2 as a transcription repressor is well characterized. However, its role during vertebrate development is still poorly understood, particularly in neurogenesis. Here, we uncover the role of EZH2 in controlling the integrity of the neural tube and allowing proper progenitor proliferation. We demonstrate that knocking down the EZH2 in chick embryo neural tubes unexpectedly disrupts the neuroepithelium (NE) structure, correlating with alteration of the Rho pathway, and reduces neural progenitor proliferation. Moreover, we use transcriptional profiling and functional assays to show that EZH2-mediated repression of p21 WAF1/CIP1 contributes to both processes. Accordingly, overexpression of cytoplasmic p21 WAF1/CIP1 induces NE structural alterations and p21 WAF1/CIP1 suppression rescues proliferation defects and partially compensates for the structural alterations and the Rho activity. Overall, our findings describe a new role of EZH2 in controlling the NE integrity in the neural tube to allow proper progenitor proliferation.

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A role for the actin cytoskeleton in the hormonal and growth-factor-mediated activation of protein kinase B

Biochemical Journal ◽

10.1042/0264-6021:3530735v ◽

2001 ◽

Vol 353 (3) ◽

pp. 735

Author(s):

K. PEYROLLIER ◽

E. HAJDUCH ◽

A. GRAY ◽

G. J. LITHERLAND ◽

A. R. PRESCOTT ◽

...

Keyword(s):

Growth Factor ◽

Protein Kinase ◽

Actin Cytoskeleton ◽

Protein Kinase B

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Spatial control of actin-based motility through plasmalemmal PtdIns(4,5)P2-rich raft assemblies.

Biochemical Society Symposium ◽

10.1042/bss0720119 ◽

2005 ◽

Vol 72 ◽

pp. 119-127 ◽

Cited By ~ 19

Author(s):

Tamara Golub ◽

Caroni Pico

Keyword(s):

Protein Kinase ◽

Cell Surface ◽

Actin Cytoskeleton ◽

Lipid Rafts ◽

Patch Clustering ◽

Pkc Protein Kinase C ◽

Membrane Bound ◽

And Function ◽

Cytoskeleton Dynamics ◽

Syndrome Protein

The interactions of cells with their environment involve regulated actin-based motility at defined positions along the cell surface. Sphingolipid- and cholesterol-dependent microdomains (rafts) order proteins at biological membranes, and have been implicated in most signalling processes at the cell surface. Many membrane-bound components that regulate actin cytoskeleton dynamics and cell-surface motility associate with PtdIns(4,5)P2-rich lipid rafts. Although raft integrity is not required for substrate-directed cell spreading, or to initiate signalling for motility, it is a prerequisite for sustained and organized motility. Plasmalemmal rafts redistribute rapidly in response to signals, triggering motility. This process involves the removal of rafts from sites that are not interacting with the substrate, apparently through endocytosis, and a local accumulation at sites of integrin-mediated substrate interactions. PtdIns(4,5)P2-rich lipid rafts can assemble into patches in a process depending on PtdIns(4,5)P2, Cdc42 (cell-division control 42), N-WASP (neural Wiskott-Aldrich syndrome protein) and actin cytoskeleton dynamics. The raft patches are sites of signal-induced actin assembly, and their accumulation locally promotes sustained motility. The patches capture microtubules, which promote patch clustering through PKA (protein kinase A), to steer motility. Raft accumulation at the cell surface, and its coupling to motility are influenced greatly by the expression of intrinsic raft-associated components that associate with the cytosolic leaflet of lipid rafts. Among them, GAP43 (growth-associated protein 43)-like proteins interact with PtdIns(4,5)P2 in a Ca2+/calmodulin and PKC (protein kinase C)-regulated manner, and function as intrinsic determinants of motility and anatomical plasticity. Plasmalemmal PtdIns(4,5)P2-rich raft assemblies thus provide powerful organizational principles for tight spatial and temporal control of signalling in motility.

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