scholarly journals Ring shape Golden Ratio multicellular structures are algebraically afforded by asymmetric mitosis and one to one cell adhesion

2018 ◽  
Author(s):  
William E. Butler ◽  
T. Bernard Kinane
Keyword(s):  
Cell Adhesion ◽  
Molecular Mechanisms ◽  
Cell Kinetics ◽  
Golden Ratio ◽  
Growth Patterns ◽  
Cell Group ◽  
Unexpected Result ◽  
Cell Groups ◽  
Cell To Cell Adhesion ◽  
Asymmetric Mitosis

AbstractGolden Ratio proportions are found throughout the world of multicellular organisms but the underlying mechanisms behind their appearance and their adaptive value if any remain unknown. The Golden Ratio is a real-valued number but cell population counts are whole numbered. Binet's formula connects the Golden Ratio to the whole numbered Fibonacci sequence (fn+1 = fn + fn–1 where f1 = 1 and f2 = 2), so we seek a cellular mechanism that yields Fibonacci cell kinetics. Drawing on Fibonacci’s description of growth patterns in rabbits, we develop a matrix model of Fibonacci cell kinetics based on an asymmetric pause between mitoses by daughter cells. We list candidate molecular mechanisms for asymmetric mitosis such as epigenetically asymmetric chromosomal sorting at anaphase due to cytosine-DNA methylation. A collection of Fibonacci-sized cell groups produced each by mitosis needs to assemble into a larger multicellular structure. We find that the mathematics for this assembly are afforded by a simple molecular cell surface configuration where each cell in each group has four cell to cell adhesion slots. Two slots internally cohere a cell group and two adhere to cells in other cell groups. We provide a notation for expressing each cell’s participation in dual Fibonacci recurrence relations. We find that single class of cell to cell adhesion molecules suffices to hold together a large assembly of chained Fibonacci groups having Golden Ratio patterns. Specialized bindings between components of various sizes are not required. Furthermore, the notation describes circumstances where chained Fibonacci-sized cell groups may leave adhesion slots unoccupied unless the chained groups anneal into a ring. This unexpected result suggests a role for Fibonacci cell kinetics in the formation of multicellular ring forms such as hollow and tubular structures. In this analysis, a complex molecular pattern behind asymmetric mitosis coordinates with a simple molecular cell adhesion pattern to generate useful multicellular assemblies. Furthermore, this reductively unifies two of the hypothesized evolutionary steps: multicellularity and cellular eusociality.

scholarly journals Cell adhesion in cancer: Beyond the migration of single cells

2020 ◽  
Vol 295 (8) ◽  
pp. 2495-2505 ◽  
Author(s):  
Michalina Janiszewska ◽  
Marina Candido Primi ◽  
Tina Izard
Keyword(s):  
Extracellular Matrix ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Molecular Mechanisms ◽  
Single Cells ◽  
Three Dimensional ◽  
Cellular Adhesion ◽  
Three Dimensional Models ◽  
Cell To Cell Adhesion

Homeostasis in healthy tissues strongly relies on cell-to-cell adhesion and cell-to-extracellular matrix interactions. For instance, normal epithelial cells maintain tissue structure by adhering to each other and to the extracellular matrix. The proteins that mediate these distinct interactions are collectively called cell adhesion molecules and are divided into four major groups: cadherins, integrins, selectins, and immunoglobulins. They not only physically anchor cells, but also critically integrate signaling between the extracellular microenvironment and cells. These signals include biochemical cues, as adhesion proteins can both act as ligand-activated receptors and activate mechanotransduction triggered by changes in the physical environment. Molecular mechanisms related to cell adhesion signaling have been extensively studied, especially because mutations and changes in expression of these proteins, particularly cadherins and integrins, are frequently associated with diseases ranging from developmental intellectual disability to cancer. In fact, two major hallmarks of cancer, loss of cell-to-cell adhesion and anchorage-independent growth, are both dependent on cell adhesion molecules. Despite many studies elucidating the relationships between malignant transformation and metastasis and cellular adhesion processes, several areas still await exploration. Here, we highlight recently discovered roles of adhesion molecules in collective cancer cell migration and discuss the utility of three-dimensional models in studying cell-cell adhesion. We also describe recent therapeutic approaches targeting adhesion molecules.

Plectin Promotes Melanoma Tumor Formation by Regulation of Src Activity

2021 ◽  
Author(s):  
Kana Mizuta ◽  
Takuma Matsubara ◽  
Akino Goto ◽  
William N. Addison ◽  
Mitsushiro Nakatomi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Adhesion ◽  
Molecular Mechanisms ◽  
Regulatory Protein ◽  
Tumor Formation ◽  
Melanoma Tumor ◽  
Efficient Treatment ◽  
Src Signaling ◽  
Cell To Cell Adhesion

Abstract Melanoma is malignant cancer characterized by high proliferation and aggressive metastasis. To address efficient treatment for melanoma, we should understand the molecular mechanisms for a proto-oncogene Src, which is highly activated and promotes cell proliferation, migration, adhesion, and metastasis in melanoma. We recently identified plectin as the Src binding protein and regulates Src activity in osteoclasts. Plectin, a cytoskeleton regulatory protein, is focused as the candidates of biomarker of certain tumors because of higher expression and the candidate of anti-tumor reagents such as ruthenium pyridinecarbothioamide although the molecular mechanisms how plectin works in melanoma is unclear. In this study, we examined the pathological role in melanoma tumor formation. Depletion of plectin induced low density and sparce tumor formation by melanoma cells in vivo. In vitro experiment revealed that plectin deficient melanomas reduced cell proliferation and suppressed cell-to-cell adhesion. Because Src activity was reduced in plectin deficient melanomas, we examined the relationship between plectin and Src signaling. Src overexpression that restored Src activity rescued cell proliferation and cell-to-cell adhesion of plectin deficient melanomas. These results suggest that plectin is required for tumor formation by promoting cell proliferation and cell-to-cell adhesion via Src signaling activity in melanoma.

ROCK2 Regulates the Expression of Cell Adhesion Molecules and Cell-to-Cell Adhesion in Vascular Endothelial Cells

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 476-P
Author(s):  
YUSUKE TAKEDA ◽  
KEIICHIRO MATOBA ◽  
DAIJI KAWANAMI ◽  
YOSUKE NAGAI ◽  
TOMOYO AKAMINE ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Cell To Cell Adhesion

scholarly journals Integrins: An Important Link between Angiogenesis, Inflammation and Eye Diseases

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1703
Author(s):  
Małgorzata Mrugacz ◽  
Anna Bryl ◽  
Mariusz Falkowski ◽  
Katarzyna Zorena
Keyword(s):  
Cell Adhesion ◽  
Tissue Repair ◽  
Normal Development ◽  
Cell Attachment ◽  
Biological Activities ◽  
Integrin Receptors ◽  
Cytokine Activation ◽  
Eye Disorders ◽  
Membrane Bound ◽  
Cell To Cell Adhesion

Integrins belong to a group of cell adhesion molecules (CAMs) which is a large group of membrane-bound proteins. They are responsible for cell attachment to the extracellular matrix (ECM) and signal transduction from the ECM to the cells. Integrins take part in many other biological activities, such as extravasation, cell-to-cell adhesion, migration, cytokine activation and release, and act as receptors for some viruses, including severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2). They play a pivotal role in cell proliferation, migration, apoptosis, tissue repair and are involved in the processes that are crucial to infection, inflammation and angiogenesis. Integrins have an important part in normal development and tissue homeostasis, and also in the development of pathological processes in the eye. This review presents the available evidence from human and animal research into integrin structure, classification, function and their role in inflammation, infection and angiogenesis in ocular diseases. Integrin receptors and ligands are clinically interesting and may be promising as new therapeutic targets in the treatment of some eye disorders.

scholarly journals Differences in a Single Extracellular Residue Underlie Adhesive Functions of Two Zebrafish Aqp0s

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2005
Author(s):  
Irene Vorontsova ◽  
James E. Hall ◽  
Thomas F. Schilling ◽  
Noriaki Nagai ◽  
Yosuke Nakazawa
Keyword(s):  
Cell Adhesion ◽  
Single Amino Acid ◽  
Amino Acid Difference ◽  
Adhesion Assay ◽  
Loss Of Function ◽  
Adhesive Properties ◽  
The Difference ◽  
In Vitro Adhesion ◽  
Cell To Cell Adhesion

Aquaporin 0 (AQP0) is the most abundant lens membrane protein, and loss of function in human and animal models leads to cataract formation. AQP0 has several functions in the lens including water transport and adhesion. Since lens optics rely on strict tissue architecture achieved by compact cell-to-cell adhesion between lens fiber cells, understanding how AQP0 contributes to adhesion would shed light on normal lens physiology and pathophysiology. We show in an in vitro adhesion assay that one of two closely related zebrafish Aqp0s, Aqp0b, has strong auto-adhesive properties while Aqp0a does not. The difference appears to be largely due to a single amino acid difference at residue 110 in the extracellular C-loop, which is T in Aqp0a and N in Aqp0b. Similarly, P110 is the key residue required for adhesion in mammalian AQP0, highlighting the importance of residue 110 in AQP0 cell-to-cell adhesion in vertebrate lenses as well as the divergence of adhesive and water permeability functions in zebrafish duplicates.

Regulation of epithelial and lymphocyte cell adhesion by adenosine deaminase–CD26 interaction

2002 ◽  
Vol 361 (2) ◽  
pp. 203-209 ◽  
Author(s):  
Silvia GINÉS ◽  
Marta MARIÑO ◽  
Josefa MALLOL ◽  
Enric I. CANELA ◽  
Chikao MORIMOTO ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Adhesion ◽  
T Cell ◽  
B Cells ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Surface ◽  
Adenosine Deaminase ◽  
Cell To Cell Adhesion ◽  
Lymphocyte Cell

The extra-enzymic function of cell-surface adenosine deaminase (ADA), an enzyme mainly localized in the cytosol but also found on the cell surface of monocytes, B cells and T cells, has lately been the subject of numerous studies. Cell-surface ADA is able to transduce co-stimulatory signals in T cells via its interaction with CD26, an integral membrane protein that acts as ADA-binding protein. The aim of the present study was to explore whether ADA—CD26 interaction plays a role in the adhesion of lymphocyte cells to human epithelial cells. To meet this aim, different lymphocyte cell lines (Jurkat and CEM T) expressing endogenous, or overexpressing human, CD26 protein were tested in adhesion assays to monolayers of colon adenocarcinoma human epithelial cells, Caco-2, which express high levels of cell-surface ADA. Interestingly, the adhesion of Jurkat and CEM T cells to a monolayer of Caco-2 cells was greatly dependent on CD26. An increase by 50% in the cell-to-cell adhesion was found in cells containing higher levels of CD26. Incubation with an anti-CD26 antibody raised against the ADA-binding site or with exogenous ADA resulted in a significant reduction (50–70%) of T-cell adhesion to monolayers of epithelial cells. The role of ADA—CD26 interaction in the lymphocyte—epithelial cell adhesion appears to be mediated by CD26 molecules that are not interacting with endogenous ADA (ADA-free CD26), since SKW6.4 (B cells) that express more cell-surface ADA showed lower adhesion than T cells. Adhesion stimulated by CD26 and ADA is mediated by T cell lymphocyte function-associated antigen. A role for ADA—CD26 interaction in cell-to-cell adhesion was confirmed further in integrin activation assays. FACS analysis revealed a higher expression of activated integrins on T cell lines in the presence of increasing amounts of exogenous ADA. Taken together, these results suggest that the ADA—CD26 interaction on the cell surface has a role in lymphocyte—epithelial cell adhesion.

Identification of Basolateral Amygdala Projection Cells and Interneurons Using Extracellular Recordings

2006 ◽  
Vol 96 (6) ◽  
pp. 3257-3265 ◽  
Author(s):  
Ekaterina Likhtik ◽  
Joe Guillaume Pelletier ◽  
Andrei T. Popescu ◽  
Denis Paré
Keyword(s):  
Firing Rate ◽  
Basolateral Amygdala ◽  
Cell Group ◽  
Small Subset ◽  
Cortical Projection ◽  
Antidromic Activation ◽  
Extracellular Recordings ◽  
Firing Rates ◽  
Cell Groups ◽  
Exact Position

This study tested whether firing rate and spike shape could be used to distinguish projection cells from interneurons in extracellular recordings of basolateral amygdala (BLA) neurons. To this end, we recorded BLA neurons in isoflurane-anesthetized animals with tungsten microelectrodes. Projection cells were identified by antidromic activation from cortical projection sites of the BLA. Although most projection cells fired spontaneously at low rates (<1 Hz), an important subset fired at higher rates (up to 6.8 Hz). In fact, the distribution of firing rates in projection cells and unidentified BLA neurons overlapped extensively, even though the latter cell group presumably contains a higher proportion of interneurons. The only difference between the two distributions was a small subset (5.1%) of unidentified neurons with unusually high firing rates (9–16 Hz). Similarly, distributions of spike durations in both cell groups were indistinguishable, although most of the fast-firing neurons had spike durations at the low end of the distribution. However, we observed that spike durations depended on the exact position of the electrode with respect to the recorded cell, varying by as much as 0.7 ms. Thus neither firing rate nor spike waveform allowed for unequivocal separation of projection cells from interneurons. Nevertheless, we propose the use of two firing rate cutoffs to obtain relatively pure samples of projection cells and interneurons: ≤1 Hz for projection cells and ≥7 Hz for fast-spiking interneurons. Supplemented with spike-duration cutoffs of ≥0.7 ms for projection cells and ≤0.5 ms for interneurons, this approach should keep instances of misclassifications to a minimum.

Molecular mechanisms involved in TFF3 peptide-mediated modulation of the E-cadherin/catenin cell adhesion complex

Peptides ◽  
2004 ◽  
Vol 25 (5) ◽  
pp. 873-883 ◽  
Author(s):  
Dirk Meyer zum Büschenfelde ◽  
Heinz Hoschützky ◽  
Rudolf Tauber ◽  
Otmar Huber
Keyword(s):  
Cell Adhesion ◽  
Molecular Mechanisms ◽  
Adhesion Complex ◽  
E Cadherin
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