Role of cell-cycle in regulating neuroepithelial cell shape during bending of the chick neural plate

1988 ◽  
Vol 252 (3) ◽  
pp. 491-500 ◽  
Author(s):  
JodiL. Smith ◽  
GaryC. Schoenwolf
Keyword(s):  
Cell Cycle ◽  
Cell Shape ◽  
Neural Plate ◽  
Neuroepithelial Cell

Cell cycle and neuroepithelial cell shape during bending of the chick neural plate

1987 ◽  
Vol 218 (2) ◽  
pp. 196-206 ◽  
Author(s):  
Jodi L. Smith ◽  
Gary C. Schoenwolf
Keyword(s):  
Cell Cycle ◽  
Cell Shape ◽  
Neural Plate ◽  
Neuroepithelial Cell

scholarly journals Redundant type II cadherins define neuroepithelial cell states for cytoarchitectonic robustness

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Kou Hiraga ◽  
Yukiko U. Inoue ◽  
Junko Asami ◽  
Mayuko Hotta ◽  
Yuki Morimoto ◽  
...  
Keyword(s):  
Cell Shape ◽  
Individual Cell ◽  
Neural Plate ◽  
Single Type ◽  
Neuroepithelial Cell ◽  
Type Ii ◽  
Double Knockout ◽  
Determine Function ◽  
Neuroepithelial Cells ◽  
Shared Roles

Abstract Individual cell shape and integrity must precisely be orchestrated during morphogenesis. Here, we determine function of type II cadherins, Cdh6, Cdh8, and Cdh11, whose expression combinatorially demarcates the mouse neural plate/tube. While CRISPR/Cas9-based single type II cadherin mutants show no obvious phenotype, Cdh6/8 double knockout (DKO) mice develop intermingled forebrain/midbrain compartments as these two cadherins’ expression opposes at the nascent boundary. Cdh6/8/11 triple, Cdh6/8 or Cdh8/11 DKO mice further cause exencephaly just within the cranial region where mutated cadherins’ expression merges. In the Cdh8/11 DKO midbrain, we observe less-constricted apical actin meshwork, ventrally-directed spreading, and occasional hyperproliferation among dorsal neuroepithelial cells as origins for exencephaly. These results provide rigid evidence that, by conferring distinct adhesive codes to each cell, redundant type II cadherins serve essential and shared roles in compartmentalization and neurulation, both of which proceed under the robust control of the number, positioning, constriction, and fluidity of neuroepithelial cells.

scholarly journals Nek8445, a protein kinase required for microtubule regulation and cytokinesis in Giardia lamblia

2019 ◽  
Author(s):  
Kelly M. Hennessey ◽  
Germain C.M. Alas ◽  
Ilse Rogiers ◽  
Renyu Li ◽  
Ethan A. Merritt ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Giardia Lamblia ◽  
Cell Shape ◽  
Cell Imaging ◽  
Microtubule Organization ◽  
General Role ◽  
Ventral Disc ◽  
Altered Cell ◽  
Fixed Cell

AbstractGiardia has 198 Nek kinases whereas humans have only 11. Giardia has a complex microtubule cytoskeleton that includes eight flagella and several unique microtubule arrays that are utilized for parasite attachment and facilitation of rapid mitosis and cytokinesis. The need to regulate these structures may explain the parallel expansion of the number of Nek family kinases. Here we use live and fixed cell imaging to uncover the role of Nek8445 in regulating Giardia cell division. We demonstrate that Nek8445 localization is cell cycle regulated and this kinase has a role in regulating overall microtubule organization. Nek8445 depletion results in short flagella, aberrant ventral disc organization, loss of the funis, defective axoneme exit and altered cell shape. The axoneme exit defect is specific to the caudal axonemes, which exit from the posterior of the cell, and this defect correlates with rounding of the cell posterior and loss of the funis. Our findings implicate a role for the funis in establishing Giardia’s cell shape and guiding axoneme docking. On a broader scale our results support the emerging view that Nek family kinases have a general role in regulating microtubule organization.

Mechanisms of neurulation: traditional viewpoint and recent advances

Development ◽  
1990 ◽  
Vol 109 (2) ◽  
pp. 243-270 ◽  
Author(s):  
G.C. Schoenwolf ◽  
J.L. Smith
Keyword(s):  
Cell Shape ◽  
Molecular Mechanisms ◽  
Review Article ◽  
Neural Plate ◽  
Neuroepithelial Cell ◽  
Morphogenetic Movements ◽  
Cell Behaviors ◽  
Recent Advances ◽  
Future Challenges ◽  
Shape Changes

In this review article, the traditional viewpoint of how neurulation occurs is evaluated in light of recent advances. This has led to the formulation of the following fundamentals: (1) neurulation, specifically neural plate shaping and bending, is a multifactorial process resulting from forces both intrinsic and extrinsic to the neural plate; (2) neurulation is driven by both changes in neuroepithelial cell shape and other form-shaping events; and (3) forces for cell shape changes are generated by both the cytoskeleton and other factors. Several cell behaviors within the neural plate have been elucidated. Future challenges include identifying cell behaviors within non-neuroepithelial tissues, determining how intrinsic and extrinsic cell behaviors are orchestrated into coordinated morphogenetic movements and elucidating the molecular mechanisms underlying such behaviors.

Biological Role of CDK 11 and 12 in Cell Cycle and its Function in Tumorigenesis

2020 ◽  
Author(s):  
Shamim Mushtaq
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Web Of Science ◽  
The Body ◽  
Main Role ◽  
Hallmarks Of Cancer ◽  
Cyclin Dependent Kinases ◽  
Tumor Studies ◽  
Cycle Regulation

Uninhibited proliferation and abnormal cell cycle regulation are the hallmarks of cancer. The main role of cyclin dependent kinases is to regulate the cell cycle and cell proliferation. These protein kinases are frequently down regulated or up regulated in various cancers. Two CDK family members, CDK 11 and 12, have contradicting views about their roles in different cancers. For example, one study suggests that the CDK 11 isoforms, p58, inhibits growth of breast cancer whereas, the CDK 11 isoform, p110, is highly expressed in breast tumor. Studies regarding CDK 12 show variation of opinion towards different parts of the body, however there is a consensus that upregulation of cdk12 increases the risk of breast cancer. Hence, CDK 11 and CDK 12 need to be analyzed to confirm their mechanism and their role regarding therapeutics, prognostic value, and ethnicity in cancer. This article gives an outline on both CDKs of information known up to date from Medline, PubMed, Google Scholar and Web of Science search engines, which were explored and thirty relevant researches were finalized.

PTTG has a Dual Role of Promotion-Inhibition in the Development of Pituitary Adenomas

2019 ◽  
Vol 26 (11) ◽  
pp. 800-818
Author(s):  
Zujian Xiong ◽  
Xuejun Li ◽  
Qi Yang
Keyword(s):  
Cell Cycle ◽  
Pituitary Adenoma ◽  
Pituitary Adenomas ◽  
Cell Cycle Progression ◽  
Key Factors ◽  
Cycle Progression ◽  
Sister Chromatids ◽  
Regulation Of Cell Cycle ◽  
Late Stages

Pituitary Tumor Transforming Gene (PTTG) of human is known as a checkpoint gene in the middle and late stages of mitosis, and is also a proto-oncogene that promotes cell cycle progression. In the nucleus, PTTG works as securin in controlling the mid-term segregation of sister chromatids. Overexpression of PTTG, entering the nucleus with the help of PBF in pituitary adenomas, participates in the regulation of cell cycle, interferes with DNA repair, induces genetic instability, transactivates FGF-2 and VEGF and promotes angiogenesis and tumor invasion. Simultaneously, overexpression of PTTG induces tumor cell senescence through the DNA damage pathway, making pituitary adenoma possessing the potential self-limiting ability. To elucidate the mechanism of PTTG in the regulation of pituitary adenomas, we focus on both the positive and negative function of PTTG and find out key factors interacted with PTTG in pituitary adenomas. Furthermore, we discuss other possible mechanisms correlate with PTTG in pituitary adenoma initiation and development and the potential value of PTTG in clinical treatment.

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