Distribution of differentiated cells in a cell sheet under the lateral inhibition rule of differentiation

1991 ◽  
Vol 153 (3) ◽  
pp. 287-300 ◽  
Author(s):  
Masaharu Tanemura ◽  
Hisao Honda ◽  
Akihiro Yoshida
Keyword(s):  
Lateral Inhibition ◽  
Cell Sheet ◽  
Differentiated Cells ◽  
A Cell

scholarly journals Mechanical bistability enabled by ectodermal compression facilitates Drosophila mesoderm invagination

2021 ◽  
Author(s):  
Hanqing Guo ◽  
Michael Swan ◽  
Shicheng Huang ◽  
Bing He
Keyword(s):  
Myosin Ii ◽  
Cell Sheet ◽  
Apical Surface ◽  
Apical Constriction ◽  
Out Of Plane ◽  
A Cell ◽  
Plane Compression ◽  
Contractile Forces ◽  
Tissue Relaxation ◽  
Muscle Myosin

Apical constriction driven by non-muscle myosin II (″myosin″) provides a well-conserved mechanism to mediate epithelial folding. It remains unclear how contractile forces near the apical surface of a cell sheet drive out-of-plane bending of the sheet and whether myosin contractility is required throughout folding. By optogenetic-mediated acute inhibition of myosin, we find that during Drosophila mesoderm invagination, myosin contractility is critical to prevent tissue relaxation during the early, ″priming″ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration, suggesting that the mesoderm is mechanically bistable during gastrulation. Combining computer modeling and experimental measurements, we show that the observed mechanical bistability arises from an in-plane compression from the surrounding ectoderm, which promotes mesoderm invagination by facilitating a buckling transition. Our results indicate that Drosophila mesoderm invagination requires a joint action of local apical constriction and global in-plane compression to trigger epithelial buckling.

Telomerase and immortalization

2019 ◽  
pp. 209-220
Author(s):  
Laura Collopy ◽  
Kazunori Tomita
Keyword(s):  
Cell Cycle ◽  
Growth And Development ◽  
Normal Cell ◽  
Chromosome Instability ◽  
Growth Arrest ◽  
Proliferative Capacity ◽  
Differentiated Cells ◽  
Dividing Cells ◽  
History Of ◽  
A Cell

The lifetime of a cell is set by the terminal ends of our chromosomes, ageing timers called telomeres. Most dividing cells, not exceptional for cancers, require telomeres to protect chromosomes. However, telomere erosion occurs at every cell cycle, thus imposing a proliferative capacity, eventually triggering a growth arrest. Cancer cells must overcome this proliferative limit in order to continue dividing. In the vast majority of cases, the growth and progression of cancers correlates with the upregulation of telomerase, an enzyme that replenishes telomeres. Telomerase is not active in normal, differentiated cells and its reactivation in cancer renders cells immortal and promotes their continued growth and development. Curiously, in cancer telomerase maintains short telomeres, retaining chromosome instability. Here, we briefly take you through history of cellular mortality with the connection to telomeres and telomerase and review their function in the normal cell to address their role during the transformation to malignancy.

Induced Pluripotent Stem Cell Elimination in a Cell Sheet by Methionine-Free and 42°C Condition for Tumor Prevention

2018 ◽  
Vol 24 (10) ◽  
pp. 605-615 ◽  
Author(s):  
Katsuhisa Matsuura ◽  
Kyoji Ito ◽  
Nobuaki Shiraki ◽  
Shoen Kume ◽  
Nobuhisa Hagiwara ◽  
...  
Keyword(s):  
Stem Cell ◽  
Pluripotent Stem Cell ◽  
Cell Sheet ◽  
Induced Pluripotent Stem Cell ◽  
Tumor Prevention ◽  
A Cell ◽  
Induced Pluripotent

scholarly journals armadillo, bazooka, and stardust are critical for early stages in formation of the zonula adherens and maintenance of the polarized blastoderm epithelium in Drosophila.

1996 ◽  
Vol 134 (1) ◽  
pp. 149-163 ◽  
Author(s):  
H A Müller ◽  
E Wieschaus
Keyword(s):  
Plasma Membranes ◽  
Basolateral Membrane ◽  
Cell Sheet ◽  
Cell Monolayer ◽  
Test System ◽  
Sem Analysis ◽  
Drosophila Embryo ◽  
Early Stages ◽  
A Cell ◽  
The Stability

Cellularization of the Drosophila embryo results in the formation of a cell monolayer with many characteristics of a polarized epithelium. We have used antibodies specific to cellular junctions and nascent plasma membranes to study the formation of the zonula adherens (ZA) in relation to the establishment of basolateral membrane polarity. The same approach was then used as a test system to identify X-linked zygotically active genes required for ZA formation. We show that ZA formation begins during cellularization and that the basolateral membrane domain is established at mid-gastrulation. By creating deficiencies for defined regions of the X chromosome, we have identified genes that are required for the formation of the ZA and the generation of basolateral membrane polarity. We show that embryos mutant for both stardust (sdt) and bazooka (baz) fail to form a ZA. In addition to the failure to establish the ZA, the formation of the monolayered epithelium is disrupted after cellularization, resulting in formation of a multilayered cell sheet by mid-gastrulation. SEM analysis of mutant embryos revealed a conversion of cells exhibiting epithelial characteristics into cells exhibiting mesenchymal characteristics. To investigate how mutations that affect an integral component of the ZA itself influence ZA formation, we examined embryos with reduced maternal and zygotic supply of wild-type Arm protein. These embryos, like embryos mutant for both sdt and baz, exhibit an early disruption of ZA formation. These results suggest that early stages in the assembly of the ZA are critical for the stability of the polarized blastoderm epithelium.

scholarly journals Cartilage Regeneration Characteristics of Human and Goat Auricular Chondrocytes

2021 ◽  
Vol 9 ◽  
Author(s):  
Mengjie Hou ◽  
Baoshuai Bai ◽  
Baoxing Tian ◽  
Zheng Ci ◽  
Yu Liu ◽  
...  
Keyword(s):  
Culture System ◽  
Cell Sheet ◽  
Cartilage Regeneration ◽  
Chondrogenic Medium ◽  
Culture Time ◽  
Medium System ◽  
A Cell ◽  
Seed Cells

Although cartilage regeneration technology has achieved clinical breakthroughs, whether auricular chondrocytes (AUCs) represent optimal seed cells to achieve stable cartilage regeneration is not clear. In this study, we systematically explore biological behaviors of human- and goat-derived AUCs during in vitro expansion as well as cartilage regeneration in vitro and in vivo. To eliminate material interference, a cell sheet model was used to evaluate the feasibility of dedifferentiated AUCs to re-differentiate and regenerate cartilage in vitro and in vivo. We found that the dedifferentiated AUCs could re-differentiate and regenerate cartilage sheets under the chondrogenic medium system, and the generated chondrocyte sheets gradually matured with increased in vitro culture time (2, 4, and 8 weeks). After the implantation of cartilage sheets with different in vitro culture times in nude mice, optimal neocartilage was formed in the group with 2 weeks in vitro cultivation. After in vivo implantation, ossification only occurred in the group with goat-regenerated cartilage sheet of 8 weeks in vitro cultivation. These results, which were confirmed in human and goat AUCs, suggest that AUCs are ideal seed cells for the clinical translation of cartilage regeneration under the appropriate culture system and culture condition.

Induction of mesenchymal stem cell differentiation by co-culturing with mature cells in double-layered 2-methacryloyloxyethyl phosphorylcholine polymer hydrogel matrices

2021 ◽  
Author(s):  
Kazuhiko Ishihara ◽  
Miu Kaneyasu ◽  
Kyoko Fukazawa ◽  
Ren Zhang ◽  
Yuji Teramura
Keyword(s):  
Stem Cell ◽  
Cell Differentiation ◽  
Stem Cell Differentiation ◽  
Water Soluble ◽  
Polymer Hydrogel ◽  
Differentiated Cells ◽  
Mesenchymal Stem Cell Differentiation ◽  
Hydrogel Matrix ◽  
Zwitterionic Polymer ◽  
A Cell

The effects of differentiated cells on stem cell differentiation were analyzed by co-culture using a cell-encapsulated double-layered hydrogel system. As a polymer hydrogel matrix, a water-soluble zwitterionic polymer having both...

scholarly journals Surface modification of uniaxial cyclic strain cell culture platform with temperature-responsive polymer for cell sheet detachment

2015 ◽  
Vol 3 (40) ◽  
pp. 7899-7902 ◽  
Author(s):  
E. L. Lee ◽  
H. H. Bendre ◽  
A. Kalmykov ◽  
J. Y. Wong
Keyword(s):  
Cell Culture ◽  
Intact Cell ◽  
Cell Sheet ◽  
Cyclic Strain ◽  
Cell Phenotype ◽  
Temperature Responsive ◽  
Current Cell ◽  
Responsive Polymer ◽  
Smooth Muscle Cell Phenotype ◽  
A Cell

Because current cell sheet-based blood vessels lack biomimetic structure and require excessively long culture times that may compromise smooth muscle cell phenotype, we modified a cell culture platform with thermoresponsive copolymers to allow intact cell sheet detachment after uniaxial conditioning.

scholarly journals Breast Cancer Stem Cells Survive Periods of Farnesyl-Transferase Inhibitor-Induced Dormancy by Undergoing Autophagy

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Moumita Chaterjee ◽  
Kenneth L. van Golen
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Metastatic Potential ◽  
Stem Cell Markers ◽  
Farnesyl Transferase ◽  
Differentiated Cells ◽  
A Cell ◽  
Cluster Of Differentiation

A cancer stem cell has been defined as a cell within a tumor that possesses the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor. These tumor-forming cells could hypothetically originate from stem, progenitor, or differentiated cells. Previously, we have shown that breast cancer cells with low metastatic potential can be induced into a reversible state of dormancy by farnesyl transferase inhibitors (FTIs). Dormancy was induced by changes in RhoA and RhoC GTPases. Specifically, RhoA was found to be hypoactivated while RhoC was hyperactivated. In the current study we demonstrate that these dormant cells also express certain known stem cell markers such as aldehyde dehydrogenase I (ALDHI) and cluster of differentiation 44 (CD44). We also show that autophagy markers Atg5, Atg12, and LC3-B are expressed in these dormant stem cell-like breast cancer cells. Inhibiting autophagy by inhibitor 3-methyladenine (3-MA) blocked the process of autophagy reversing the dormant phenotype. Further, we show that c-jun NH2 terminal kinase (JNK/SAPK) is upregulated in these dormant stem cell-like breast cancer cells and is responsible for increasing autophagy.

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