Endocytosis, cadherins and tissue dynamics

Katsuno-Kambe, Hiroko; Yap, Alpha

doi:10.1111/tra.12721

Cited by 17 publications

(11 citation statements)

References 39 publications

(79 reference statements)

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“…Historically, there have been different perspectives on how to understand and quantify such rearrangements. At the molecular scale, a concerted sequence of processes must occur to allow such a change, including localization of non-muscle myosin and actin to shorten interfaces [6][7][8][9][10], unbinding of adhesion molecules and trafficking away from the membrane via endocytosis [11], exocytosis of adhesion molecules to newly formed interfaces and new homotypic binding, and reorganization of the cytoskeleton to stabilize the new edges. Moreover, molecules such as tricellulin [12,13] are known to localize at tricellular junctions and must be reorganized [14,15].…”

Section: Introductionmentioning

confidence: 99%

Effect of cellular rearrangement time delays on the rheology of vertex models for confluent tissues

Erdemci-Tandogan

Manning

2021

PLoS Comput Biol

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Large-scale tissue deformation during biological processes such as morphogenesis requires cellular rearrangements. The simplest rearrangement in confluent cellular monolayers involves neighbor exchanges among four cells, called a T1 transition, in analogy to foams. But unlike foams, cells must execute a sequence of molecular processes, such as endocytosis of adhesion molecules, to complete a T1 transition. Such processes could take a long time compared to other timescales in the tissue. In this work, we incorporate this idea by augmenting vertex models to require a fixed, finite time for T1 transitions, which we call the “T1 delay time”. We study how variations in T1 delay time affect tissue mechanics, by quantifying the relaxation time of tissues in the presence of T1 delays and comparing that to the cell-shape based timescale that characterizes fluidity in the absence of any T1 delays. We show that the molecular-scale T1 delay timescale dominates over the cell shape-scale collective response timescale when the T1 delay time is the larger of the two. We extend this analysis to tissues that become anisotropic under convergent extension, finding similar results. Moreover, we find that increasing the T1 delay time increases the percentage of higher-fold coordinated vertices and rosettes, and decreases the overall number of successful T1s, contributing to a more elastic-like—and less fluid-like—tissue response. Our work suggests that molecular mechanisms that act as a brake on T1 transitions could stiffen global tissue mechanics and enhance rosette formation during morphogenesis.

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Section: Introductionmentioning

confidence: 99%

Effect of cellular rearrangement time delays on the rheology of vertex models for confluent tissues

Erdemci-Tandogan

Manning

2021

PLoS Comput Biol

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“…Although these activities are largely pertinent to the workings of individual cells, it is becoming increasingly clear that also cellular collectives are controlled by endocytosis. This is remarkable, as it entails that endocytic events occurring on the level of a single cell must be synchronized, frequently spanning a distance of hundreds of cells, to contribute to a coordinated behaviour [10][11][12][13] .…”

mentioning

confidence: 99%

“…In this Review, we discuss the pleiotropic roles of endocytosis in cell regulation and the importance of these mechanisms in physiology and pathology, especially cancer. Many of these facets of endocytosis have been excellently reviewed elsewhere [5][6][7][10][11][12][13] .…”

mentioning

confidence: 99%

Endocytosis in the context-dependent regulation of individual and collective cell properties

Sigismund

Lanzetti

Scita

et al. 2021

Nat Rev Mol Cell Biol

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Endocytosis allows cells to transport particles and molecules across the plasma membrane. In addition, it is involved in the termination of signalling through receptor downmodulation and degradation. This "traditional" outlook has been substantially modified, in recent years, by discoveries that endocytosis and subsequent trafficking routes have a profound impact on the positive regulation and propagation of signals, being key for spatio-temporal regulation of signal transmission in cells. Accordingly, endocytosis and membrane traffic regulate virtually every aspect of cell physiology, and are frequently subverted in pathological conditions. Two key aspects of endocytic control over signalling are coming into focus: context-dependency and long-range effects. First, endocytic-regulated outputs are not stereotyped, but heavily dependent on cell-specific regulation of endocytic networks. Second, endocytic regulation has impact not only on individual cells, but also on the behaviour of cellular collectives. Herein, we will discuss recent advancements in these areas, highlighting how endocytic trafficking impacts complex cell properties, including cell polarity and collective cell migration, and the relevance of these mechanisms to disease, in particular cancer. [H1] IntroductionEndocytosis is used by cells to internalize various types of molecules, including nutrients, and fluids, which could not otherwise pass through the plasma membrane 1,2 . While this has probably represented the initial driving force behind its emergence in evolution, the system has been exploited to actively regulate various forms of communication within the cell and between the cell and its environment. Signalling receptors, for instance, are internalized upon engagement by cognate ligands and frequently targeted for degradation in the lysosome, resulting in long-term signalling attenuation 3,4 . In addition, regardless of their interaction with extracellular moieties, many surface-resident molecules (mostly, but not exclusively, proteins) are

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Section: Box 1 Hallmarks Of Emtmentioning

confidence: 99%

“…While transcriptional inhibition ensures that no new junctions are formed, active removal of cadherin molecules from the cell surface ensures that existing junctions are broken down. This removal occurs through endocytosis, followed by lysosomal degradation of the cadherins, which normally undergo recycling [145,146]. An international consortium of researchers recently published guidelines to investigate and define the EMT process, and its many intermediate phenotypes, based on a combination of molecular markers and cellular properties [147].…”

Section: Experimental Evidence For Interplay Of the Ctnnb1 Poolsmentioning

confidence: 99%

Walking the tight wire between cell adhesion and WNT signalling: a balancing act for β-catenin

Wal

Amerongen

2020

Open Biol.

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CTNNB1 (catenin β-1, also known as β-catenin) plays a dual role in the cell. It is the key effector of WNT/CTNNB1 signalling, acting as a transcriptional co-activator of TCF/LEF target genes. It is also crucial for cell adhesion and a critical component of cadherin-based adherens junctions. Two functional pools of CTNNB1, a transcriptionally active and an adhesive pool, can therefore be distinguished. Whether cells merely balance the distribution of available CTNNB1 between these functional pools or whether interplay occurs between them has long been studied and debated. While interplay has been indicated upon artificial modulation of cadherin expression levels and during epithelial–mesenchymal transition, it is unclear to what extent CTNNB1 exchange occurs under physiological conditions and in response to WNT stimulation. Here, we review the available evidence for both of these models, discuss how CTNNB1 binding to its many interaction partners is controlled and propose avenues for future studies.

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Endocytosis, cadherins and tissue dynamics

Cited by 17 publications

References 39 publications

Effect of cellular rearrangement time delays on the rheology of vertex models for confluent tissues

Effect of cellular rearrangement time delays on the rheology of vertex models for confluent tissues

Endocytosis in the context-dependent regulation of individual and collective cell properties

Walking the tight wire between cell adhesion and WNT signalling: a balancing act for β-catenin

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