scholarly journals Rab5ab-Mediated Yolk Cell Membrane Endocytosis Is Essential for Zebrafish Epiboly and Mechanical Equilibrium During Gastrulation

2021 ◽  
Vol 9 ◽  
Author(s):  
Maria Marsal ◽  
Amayra Hernández-Vega ◽  
Philippe-Alexandre Pouille ◽  
Enrique Martin-Blanco
Keyword(s):  
Tissue Mechanics ◽  
Force Balance ◽  
Membrane Remodeling ◽  
Internal Flows ◽  
Membrane Turnover ◽  
Morphogenetic Movements ◽  
Yolk Cell ◽  
Final Destination ◽  
Early Embryos ◽  
Spatio Temporal

Morphogenesis in early embryos demands the coordinated distribution of cells and tissues to their final destination in a spatio-temporal controlled way. Spatial and scalar differences in adhesion and contractility are essential for these morphogenetic movements, while the role that membrane remodeling may play remains less clear. To evaluate how membrane turnover modulates tissue arrangements we studied the role of endocytosis in zebrafish epiboly. Experimental analyses and modeling have shown that the expansion of the blastoderm relies on an asymmetry of mechanical tension in the yolk cell generated as a result of actomyosin-dependent contraction and membrane removal. Here we show that the GTPase Rab5ab is essential for the endocytosis and the removal of the external yolk cell syncytial layer (E-YSL) membrane. Interfering in its expression exclusively in the yolk resulted in the reduction of yolk cell actomyosin contractility, the disruption of cortical and internal flows, a disequilibrium in force balance and epiboly impairment. We conclude that regulated membrane remodeling is crucial for directing cell and tissue mechanics, preserving embryo geometry and coordinating morphogenetic movements during epiboly.

scholarly journals Rab5-mediated Yolk Cell Endocytosis modulates Zebrafish Epiboly Biomechanics and Tissue Movements

2016 ◽  
Author(s):  
Maria Marsal ◽  
Amayra Hernández-Vega ◽  
Philippe-Alexandre Pouille ◽  
Enrique Martin-Blanco
Keyword(s):  
Tissue Mechanics ◽  
Force Balance ◽  
Zebrafish Embryos ◽  
Membrane Remodeling ◽  
Mechanical Tension ◽  
Morphogenetic Movements ◽  
Yolk Cell ◽  
Final Destination ◽  
Actomyosin Contractility ◽  
Spatio Temporal

SummaryMorphogenetic processes demand the coordinated allocation of cells and tissues to their final destination in a spatio-temporal controlled way. Identifying how these morphogenetic movements are directed and implemented is essential for understanding morphogenesis. Topographical and scalar differences in adhesion and contractility within and between cells are essential, yet, the role that membrane remodeling may play remains less clear. To clarify how surface turnover and dynamics may modulate tissue arrangements we studied epiboly in the zebrafish. During epiboly the blastoderm expands as a result of an asymmetry of mechanical tension along the embryo surface. In this scenario, we found that the membrane removal by macropinocytosis of the external yolk cell syncytial layer (E-YSL) ahead of the blastoderm is key for epiboly progression In early zebrafish embryos, the activity of the GTPase Rab5ab was essential for endocytosis, and interference in its expression exclusively in the yolk cell resulted in the reduction of yolk cell actomyosin contractility, the disruption of cortical and internal yolk flows, a disequilibrium in force balance and as a result epiboly impairment. We conclude that regulated membrane remodeling is crucial for directing cell and tissue mechanics and coordinating morphogenetic movements during epiboly.

scholarly journals Simultaneous in vivo time-lapse stiffness mapping and fluorescence imaging of developing tissue

2018 ◽  
Author(s):  
Amelia J. Thompson ◽  
Iva K. Pillai ◽  
Ivan B. Dimov ◽  
Christine E. Holt ◽  
Kristian Franze
Keyword(s):  
Fluorescence Imaging ◽  
Temporal Dynamics ◽  
Time Lapse ◽  
Tissue Mechanics ◽  
Tissue Stiffness ◽  
Time Resolved ◽  
Force Microscopy ◽  
Atomic Force ◽  
Spatio Temporal

AbstractTissue mechanics is important for development; however, the spatio-temporal dynamics of in vivo tissue stiffness is still poorly understood. We here developed tiv-AFM, combining time-lapse in vivo atomic force microscopy with upright fluorescence imaging of embryonic tissue, to show that in the developing Xenopus brain, a stiffness gradient evolves over time because of differential cell proliferation. Subsequently, axons turn to follow this gradient, underpinning the importance of time-resolved mechanics measurements.

scholarly journals Getting to know your neighbor: Cell polarization in early embryos

2014 ◽  
Vol 206 (7) ◽  
pp. 823-832 ◽  
Author(s):  
Jeremy Nance
Keyword(s):  
Cell Fate ◽  
Cell Polarization ◽  
Cell Contact ◽  
Cell Fates ◽  
Par Proteins ◽  
Morphogenetic Movements ◽  
Cell Fate Decisions ◽  
Contact Patterns ◽  
Early Embryos ◽  
Contact Free

Polarization of early embryos along cell contact patterns—referred to in this paper as radial polarization—provides a foundation for the initial cell fate decisions and morphogenetic movements of embryogenesis. Although polarity can be established through distinct upstream mechanisms in Caenorhabditis elegans, Xenopus laevis, and mouse embryos, in each species, it results in the restriction of PAR polarity proteins to contact-free surfaces of blastomeres. In turn, PAR proteins influence cell fates by affecting signaling pathways, such as Hippo and Wnt, and regulate morphogenetic movements by directing cytoskeletal asymmetries.

scholarly journals Fibronectin-dependent tissue mechanics regulate the translation of segmentation clock oscillations into periodic somite formation

2019 ◽  
Author(s):  
Patrícia Gomes de Almeida ◽  
Pedro Rifes ◽  
Ana Patrícia Martins-Jesus ◽  
Gonçalo G. Pinheiro ◽  
Raquel P. Andrade ◽  
...  
Keyword(s):  
Gene Expression ◽  
Clock Gene ◽  
Clock Genes ◽  
Tissue Mechanics ◽  
Matrix Assembly ◽  
Segmentation Clock ◽  
Clock Gene Expression ◽  
Fibronectin Matrix ◽  
Somite Formation ◽  
Spatio Temporal

AbstractSomitogenesis starts with cyclic waves of expression of segmentation clock genes in the presomitic mesoderm (PSM) and culminates with periodic budding of somites in its anterior-most region. How cyclic clock gene expression is translated into timely morphological somite formation has remained unclear. A posterior to anterior gradient of increasing PSM tissue cohesion correlates with increasing fibronectin matrix complexity around the PSM, suggesting that fibronectin-dependent tissue mechanics may be involved in this transition. Here we address whether the mechanical properties of the PSM tissue play a role in regulating the pathway leading to cleft formation in the anterior PSM. We first interfered with cytoskeletal contractility in the chick PSM by disrupting actomyosin-mediated contractility directly or via Rho-associated protein kinase function. Then we perturbed fibronectin matrix accumulation around the PSM tissue by blocking integrin-fibronectin binding or fibronectin matrix assembly. All four treatments perturbed hairy1 and meso1 expression dynamics and resulted in defective somitic clefts. A model is presented where a gradient of fibronectin-dependent tissue mechanics participates in the PSM wavefront of maturation by ensuring the correct spatio-temporal conversion of cyclic segmentation clock gene expression into periodic somite formation.

scholarly journals Network architecture determines vein fate during spontaneous reorganization, with a time delay

2021 ◽  
Author(s):  
Sophie Marbach ◽  
Noah Ziethen ◽  
Leonie Bastin ◽  
Felix Baeuerle ◽  
Karen Alim
Keyword(s):  
Time Delay ◽  
Network Architecture ◽  
Force Balance ◽  
Relative Pressure ◽  
Temporal Data ◽  
Vascular Networks ◽  
Local Shear ◽  
Flow Shear Stress ◽  
Spatio Temporal

Vascular networks continuously reorganize their morphology by growing new or shrinking existing veins to optimize function. Flow shear stress on vein walls has been set forth as the local driver for this continuous adaptation. Yet, shear feedback alone cannot account for the observed diversity of network dynamics -- a puzzle made harder by scarce spatio-temporal data. Here, we resolve network-wide vein dynamics and shear during spontaneous reorganization in the prototypical vascular networks of Physarum polycephalum. Our experiments reveal a plethora of vein dynamics (stable, growing, shrinking) that are not directly proportional to local shear. We observe (a) that shear rate sensing on vein walls occurs with a time delay of 1 to 3 min and (b) that network architecture dependent parameters -- such as relative pressure or relative vein resistance -- are key to determine vein fate. We derive a model for vascular adaptation, based on force balance at the vein walls. Together with the time delay, our model reproduces the diversity of experimentally observed vein dynamics, and confirms the role of network architecture. Finally, we observe avalanches of network reorganization events which cause entire clusters of veins to vanish. Such avalanches are consistent with architectural feedback as the vein connections perpetually change with reorganization. As these network architecture dependent parameters are intrinsically connected with the laminar fluid flow in the veins, we expect our findings to play a role across flow-based vascular networks.

scholarly journals The desmoplakin–intermediate filament linkage regulates cell mechanics

2017 ◽  
Vol 28 (23) ◽  
pp. 3156-3164 ◽  
Author(s):  
Joshua A. Broussard ◽  
Ruiguo Yang ◽  
Changjin Huang ◽  
S. Shiva P. Nathamgari ◽  
Allison M. Beese ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Cell Mechanics ◽  
Intermediate Filament ◽  
Tissue Mechanics ◽  
Force Balance ◽  
Cell Stiffness ◽  
Inherited Disorders ◽  
Physiological Processes ◽  
Network Composition ◽  
Mutant Forms

The translation of mechanical forces into biochemical signals plays a central role in guiding normal physiological processes during tissue development and homeostasis. Interfering with this process contributes to cardiovascular disease, cancer progression, and inherited disorders. The actin-based cytoskeleton and its associated adherens junctions are well-established contributors to mechanosensing and transduction machinery; however, the role of the desmosome–intermediate filament (DSM–IF) network is poorly understood in this context. Because a force balance among different cytoskeletal systems is important to maintain normal tissue function, knowing the relative contributions of these structurally integrated systems to cell mechanics is critical. Here we modulated the interaction between DSMs and IFs using mutant forms of desmoplakin, the protein bridging these structures. Using micropillar arrays and atomic force microscopy, we demonstrate that strengthening the DSM–IF interaction increases cell–substrate and cell–cell forces and cell stiffness both in cell pairs and sheets of cells. In contrast, disrupting the interaction leads to a decrease in these forces. These alterations in cell mechanics are abrogated when the actin cytoskeleton is dismantled. These data suggest that the tissue-specific variability in DSM–IF network composition provides an opportunity to differentially regulate tissue mechanics by balancing and tuning forces among cytoskeletal systems.

scholarly journals Rapid changes in tissue mechanics regulate cell behaviour in the developing embryonic brain

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Amelia J Thompson ◽  
Eva K Pillai ◽  
Ivan B Dimov ◽  
Sarah K Foster ◽  
Christine E Holt ◽  
...  
Keyword(s):  
Temporal Dynamics ◽  
Time Lapse ◽  
Time Frame ◽  
Tissue Mechanics ◽  
Tissue Stiffness ◽  
Time Resolved ◽  
Local Tissue ◽  
Close Relationship ◽  
Spatio Temporal

Tissue mechanics is important for development; however, the spatio-temporal dynamics of in vivo tissue stiffness is still poorly understood. We here developed tiv-AFM, combining time-lapse in vivo atomic force microscopy with upright fluorescence imaging of embryonic tissue, to show that during development local tissue stiffness changes significantly within tens of minutes. Within this time frame, a stiffness gradient arose in the developing Xenopus brain, and retinal ganglion cell axons turned to follow this gradient. Changes in local tissue stiffness were largely governed by cell proliferation, as perturbation of mitosis diminished both the stiffness gradient and the caudal turn of axons found in control brains. Hence, we identified a close relationship between the dynamics of tissue mechanics and developmental processes, underpinning the importance of time-resolved stiffness measurements.

scholarly journals Passive myocardial mechanical properties: meaning, measurement, models

2021 ◽  
Vol 13 (5) ◽  
pp. 587-610
Author(s):  
Ramona Emig ◽  
Callum M. Zgierski-Johnston ◽  
Viviane Timmermann ◽  
Andrew J. Taberner ◽  
Martyn P. Nash ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Myocardial Contraction ◽  
Experimental Models ◽  
Tissue Mechanics ◽  
Tissue Properties ◽  
Measurement Models ◽  
Spatio Temporal ◽  
Mechanical Tissue

AbstractPassive mechanical tissue properties are major determinants of myocardial contraction and relaxation and, thus, shape cardiac function. Tightly regulated, dynamically adapting throughout life, and affecting a host of cellular functions, passive tissue mechanics also contribute to cardiac dysfunction. Development of treatments and early identification of diseases requires better spatio-temporal characterisation of tissue mechanical properties and their underlying mechanisms. With this understanding, key regulators may be identified, providing pathways with potential to control and limit pathological development. Methodologies and models used to assess and mimic tissue mechanical properties are diverse, and available data are in part mutually contradictory. In this review, we define important concepts useful for characterising passive mechanical tissue properties, and compare a variety of in vitro and in vivo techniques that allow one to assess tissue mechanics. We give definitions of key terms, and summarise insight into determinants of myocardial stiffness in situ. We then provide an overview of common experimental models utilised to assess the role of environmental stiffness and composition, and its effects on cardiac cell and tissue function. Finally, promising future directions are outlined.

Changes Occur in Plasma Membrane Turnover when K562 Leukemia Cells are Induced to Differentiate

1982 ◽  
Vol 40 ◽  
pp. 286-287
Author(s):  
L. M. Marshall
Keyword(s):  
Plasma Membrane ◽  
Membrane Proteins ◽  
Intracellular Transport ◽  
Parent Cell ◽  
Membrane Turnover ◽  
Coated Pits ◽  
Surface Distribution ◽  
Specific Proteins ◽  
Erythroleukemic Cell ◽  
Specific Membrane

A human erythroleukemic cell line, metabolically blocked in a late stage of erythropoiesis, becomes capable of differentiation along the normal pathway when grown in the presence of hemin. This process is characterized by hemoglobin synthesis followed by rearrangement of the plasma membrane proteins and culminates in asymmetrical cytokinesis in the absence of nuclear division. A reticulocyte-like cell buds from the nucleus-containing parent cell after erythrocyte specific membrane proteins have been sequestered into its membrane. In this process the parent cell faces two obstacles. First, to organize its erythrocyte specific proteins at one pole of the cell for inclusion in the reticulocyte; second, to reduce or abolish membrane protein turnover since hemoglobin is virtually the only protein being synthesized at this stage. A means of achieving redistribution and cessation of turnover could involve movement of membrane proteins by a directional lipid flow. Generation of a lipid flow towards one pole and accumulation of erythrocyte-specific membrane proteins could be achieved by clathrin coated pits which are implicated in membrane endocytosis, intracellular transport and turnover. In non-differentiating cells, membrane proteins are turned over and are random in surface distribution. If, however, the erythrocyte specific proteins in differentiating cells were excluded from endocytosing coated pits, not only would their turnover cease, but they would also tend to drift towards and collect at the site of endocytosis. This hypothesis requires that different protein species are endocytosed by the coated vesicles in non-differentiating than by differentiating cells.

E3 ubiquitin ligases

2005 ◽  
Vol 41 ◽  
pp. 15-30 ◽  
Author(s):  
Helen C. Ardley ◽  
Philip A. Robinson
Keyword(s):  
Protein Complexes ◽  
Loss Of Function ◽  
Direct Role ◽  
Cellular Processes ◽  
Substrate Protein ◽  
Protein Ubiquitination ◽  
C Terminus ◽  
Full Complement ◽  
Spatio Temporal ◽  
Eukaryotic Organisms

The selectivity of the ubiquitin–26 S proteasome system (UPS) for a particular substrate protein relies on the interaction between a ubiquitin-conjugating enzyme (E2, of which a cell contains relatively few) and a ubiquitin–protein ligase (E3, of which there are possibly hundreds). Post-translational modifications of the protein substrate, such as phosphorylation or hydroxylation, are often required prior to its selection. In this way, the precise spatio-temporal targeting and degradation of a given substrate can be achieved. The E3s are a large, diverse group of proteins, characterized by one of several defining motifs. These include a HECT (homologous to E6-associated protein C-terminus), RING (really interesting new gene) or U-box (a modified RING motif without the full complement of Zn2+-binding ligands) domain. Whereas HECT E3s have a direct role in catalysis during ubiquitination, RING and U-box E3s facilitate protein ubiquitination. These latter two E3 types act as adaptor-like molecules. They bring an E2 and a substrate into sufficiently close proximity to promote the substrate's ubiquitination. Although many RING-type E3s, such as MDM2 (murine double minute clone 2 oncoprotein) and c-Cbl, can apparently act alone, others are found as components of much larger multi-protein complexes, such as the anaphase-promoting complex. Taken together, these multifaceted properties and interactions enable E3s to provide a powerful, and specific, mechanism for protein clearance within all cells of eukaryotic organisms. The importance of E3s is highlighted by the number of normal cellular processes they regulate, and the number of diseases associated with their loss of function or inappropriate targeting.

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