scholarly journals A unique form of collective epithelial migration is crucial for tissue fusion in the secondary palate and can overcome loss of epithelial apoptosis

2021 ◽  
Author(s):  
Teng Teng ◽  
Camilla Teng ◽  
Vesa Kaartinen ◽  
Jeffrey O. Bush
Keyword(s):  
Live Imaging ◽  
Tissue Fusion ◽  
Unique Form ◽  
Cellular Mechanisms ◽  
Epithelial Migration ◽  
Actomyosin Contractility ◽  
Secondary Palate ◽  
Epithelial Marker ◽  
Peristaltic Movement ◽  
Cell Extrusion

AbstractTissue fusion is an oft-employed process in morphogenesis which often requires the removal of the epithelia intervening multiple distinct primordia to form one continuous structure. In the mammalian secondary palate, a midline epithelial seam (MES) forms between two palatal shelves and must be removed to allow mesenchymal confluence. Abundant apoptosis and cell extrusion in this epithelial seam support their importance in its removal. However, by genetically disrupting the intrinsic apoptotic regulators BAX and BAK within the MES, we find a complete loss of cell death and cell extrusion, but successful removal of the MES, indicating that developmental compensation enables fusion. Novel static and live imaging approaches reveal that the MES is removed through a unique form of collective epithelial cell migration in which epithelial trails and islands stream through the mesenchyme to reach the oral and nasal epithelial surfaces. These epithelial trails and islands begin to express periderm markers while retaining expression of the basal epithelial marker ΔNp63, suggesting their migration to the oral and nasal surface is concomitant with their differentiation to an epithelial intermediate. Live imaging reveals anisotropic actomyosin contractility within epithelial trails that drives their peristaltic movement, and genetic loss of non-muscle myosin IIA-mediated actomyosin contractility results in dispersion of epithelial collectives and dramatic failure of normal MES migration. These findings demonstrate redundancy between cellular mechanisms of morphogenesis and reveal a crucial role for a unique form of collective epithelial migration during tissue fusion.

scholarly journals Watching a deep dive: Live imaging provides lessons about tooth invagination

2016 ◽  
Vol 214 (6) ◽  
pp. 645-647 ◽  
Author(s):  
Amnon Sharir ◽  
Ophir D. Klein
Keyword(s):  
Live Imaging ◽  
Cellular Mechanisms ◽  
Deep Dive ◽  
Critical Step ◽  
Organ Morphogenesis ◽  
Cell Biol ◽  
Mouse Incisor

Invagination of epithelium into the surrounding mesenchyme is a critical step that marks the developmental onset of many ectodermal organs. In this issue, Ahtiainen et al. (2016. J. Cell. Biol. http://dx.doi.org/10.1083/jcb.201512074) use the mouse incisor as a model to advance our understanding of the cellular mechanisms underlying ectodermal organ morphogenesis.

scholarly journals Iron elevates mesenchymal and metastatic biomarkers in HepG2 cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Kosha J. Mehta ◽  
Paul A. Sharp
Keyword(s):  
Transcription Factors ◽  
Mrna Expression ◽  
Hepg2 Cells ◽  
Cellular Mechanisms ◽  
Intracellular Iron ◽  
Liver Iron ◽  
Mesenchymal Transition ◽  
Excess Iron ◽  
Epithelial Marker ◽  
E Cadherin

AbstractLiver iron excess is observed in several chronic liver diseases and is associated with the development of hepatocellular carcinoma (HCC). However, apart from oxidative stress, other cellular mechanisms by which excess iron may mediate/increase HCC predisposition/progression are not known. HCC pathology involves epithelial to mesenchymal transition (EMT), the basis of cancer phenotype acquisition. Here, the effect of excess iron (holo-transferrin 0–2 g/L for 24 and 48 h) on EMT biomarkers in the liver-derived HepG2 cells was investigated. Holo-transferrin substantially increased intracellular iron. Unexpectedly, mRNA and protein expression of the epithelial marker E-cadherin either remained unaltered or increased. The mRNA and protein levels of metastasis marker N-cadherin and mesenchymal marker vimentin increased significantly. While the mRNA expression of EMT transcription factors SNAI1 and SNAI2 increased and decreased, respectively after 24 h, both factors increased after 48 h. The mRNA expression of TGF-β (EMT-inducer) showed no significant alterations. In conclusion, data showed direct link between iron and EMT. Iron elevated mesenchymal and metastatic biomarkers in HepG2 cells without concomitant decrement in the epithelial marker E-cadherin and altered the expression of the key EMT-mediating transcription factors. Such studies can help identify molecular targets to devise iron-related adjunctive therapies to ameliorate HCC pathophysiology.

scholarly journals Concerted action of neuroepithelial basal shrinkage and active epithelial migration ensures efficient optic cup morphogenesis

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Jaydeep Sidhaye ◽  
Caren Norden
Keyword(s):  
Tissue Level ◽  
Cellular Mechanisms ◽  
Epithelial Migration ◽  
Multi Scale ◽  
Cell Matrix ◽  
Optic Cup ◽  
Correct Location ◽  
Spatiotemporal Coordination ◽  
Cellular Movement

Organ formation is a multi-scale event that involves changes at the intracellular, cellular and tissue level. Organogenesis often starts with the formation of characteristically shaped organ precursors. However, the cellular mechanisms driving organ precursor formation are often not clear. Here, using zebrafish, we investigate the epithelial rearrangements responsible for the development of the hemispherical retinal neuroepithelium (RNE), a part of the optic cup. We show that in addition to basal shrinkage of RNE cells, active migration of connected epithelial cells into the RNE is a crucial player in its formation. This cellular movement is driven by progressive cell-matrix contacts and actively translocates prospective RNE cells to their correct location before they adopt neuroepithelial fate. Failure of this migration during neuroepithelium formation leads to ectopic determination of RNE cells and consequently impairs optic cup formation. Overall, this study illustrates how spatiotemporal coordination between morphogenic movements and fate determination critically influences organogenesis.

scholarly journals Cephalopod Retinal Development Shows Vertebrate-like Mechanisms of Neurogenesis

2021 ◽  
Author(s):  
Francesca Napoli ◽  
Christina M Daly ◽  
Stephanie Neal ◽  
Kyle J McCulloch ◽  
Alexandra Zaloga ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Nervous System ◽  
Progenitor Cells ◽  
Cellular Proliferation ◽  
Imaging Techniques ◽  
Nuclear Migration ◽  
Live Imaging ◽  
Cellular Mechanisms ◽  
High Resolution Data ◽  
Interkinetic Nuclear Migration

Neurogenesis, the regulation of cellular proliferation and differentiation in the developing nervous system, is the process that underlies the diversity of size and cell type found in animal nervous systems. Our understanding of how this process has evolved is limited because of the lack of high resolution data and live-imaging methods across species. The retina is a classic model for the study of neurogenesis in vertebrates and live-imaging of the retina has shown that during development, progenitor cells are organized in a pseudostratified neuroepithelium and nuclei migrate in coordination with the cell cycle along the apicobasal axis of the cell, a process called interkinetic nuclear migration. Eventually cells delaminate and differentiate within the boundaries of the epithelium. This process has been considered unique to vertebrates and thought to be important in maintaining organization during the development of a complex nervous system. Coleoid cephalopods, including squid, cuttlefish and octopus, have the largest nervous system of any invertebrate and convergently-evolved camera-type eyes, making them a compelling comparative system to vertebrates. Here we have pioneered live-imaging techniques to show that the squid, Doryteuthis pealeii, displays cellular mechanisms during cephalopod retinal neurogenesis that are hallmarks of vertebrate processes. We find that retinal progenitor cells in the squid undergo interkinetic nuclear migration until they exit the cell cycle, we identify retinal organization corresponding to progenitor, post-mitotic and differentiated cells, and we find that Notch signaling regulates this process. With cephalopods and vertebrates having diverged 550 million years ago, these results suggest that mechanisms thought to be unique to vertebrates may be common to highly proliferative neurogenic primordia contributing to a large nervous system.

scholarly journals Molecular and Cellular Mechanisms of Palate Development

2017 ◽  
Vol 96 (11) ◽  
pp. 1184-1191 ◽  
Author(s):  
C. Li ◽  
Y. Lan ◽  
R. Jiang
Keyword(s):  
Growth Factor ◽  
Regulatory Networks ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Cellular Mechanisms ◽  
Palate Development ◽  
Palatal Shelf ◽  
Cellular Processes ◽  
Morphogenetic Protein ◽  
Secondary Palate

Development of the mammalian secondary palate involves highly dynamic morphogenetic processes, including outgrowth of palatal shelves from the oral side of the embryonic maxillary prominences, elevation of the initially vertically oriented palatal shelves to the horizontal position above the embryonic tongue, and subsequently adhesion and fusion of the paired palatal shelves at the midline to separate the oral cavity from the nasal cavity. Perturbation of any of these processes could cause cleft palate, a common birth defect that significantly affects patients’ quality of life even after surgical treatment. In addition to identifying a large number of genes required for palate development, recent studies have begun to unravel the extensive cross-regulation of multiple signaling pathways, including Sonic hedgehog, bone morphogenetic protein, fibroblast growth factor, transforming growth factor β, and Wnt signaling, and multiple transcription factors during palatal shelf growth and patterning. Multiple studies also provide new insights into the gene regulatory networks and/or dynamic cellular processes underlying palatal shelf elevation, adhesion, and fusion. Here we summarize major recent advances and integrate the genes and molecular pathways with the cellular and morphogenetic processes of palatal shelf growth, patterning, elevation, adhesion, and fusion.

scholarly journals Live Imaging of Mouse Secondary Palate Fusion

10.3791/56041 ◽  
2017 ◽  
Author(s):  
Seungil Kim ◽  
Jan Prochazka ◽  
Jeffrey O. Bush
Keyword(s):  
Live Imaging ◽  
Secondary Palate

scholarly journals Desmosomal coupling in apoptotic cell extrusion

2019 ◽  
Author(s):  
Minnah Thomas ◽  
Benoit Ladoux ◽  
Yusuke Toyama
Keyword(s):  
De Novo ◽  
Apoptotic Cell ◽  
Cell Junctions ◽  
Dead Cell ◽  
Mechanical Coupling ◽  
Physiological Processes ◽  
Actomyosin Contractility ◽  
Epithelial Sheet ◽  
Dying Cells ◽  
Cell Extrusion

SUMMARYThe mechanical coupling of epithelia enables coordination of tissue functions and collective tissue movements during different developmental and physiological processes. This coupling is ensured by cell-cell junctions, including adherens junctions (AJs) and desmosomal junctions (DJs) [1, 2]. During apoptosis, or programmed cell death, a dead cell is expelled from the tissue by coordinated processes between the dying cell and its neighbors. Apoptotic cell extrusion is driven by actomyosin cable formation and its contraction, and lamellipodial crawling of the neighboring cells (Fig. S1A-A’’, Movie S1) [3–6]. Throughout cell extrusion, the mechanical coupling of epithelia needs to be maintained in order to preserve tissue homeostasis [3]. Although much is known about the regulation of AJs in apoptotic cell extrusion [6–9], the role and dynamics of DJs during this process remains poorly understood. Here, we show that DJs stay intact throughout and are crucial for apoptotic cell extrusion. Pre-existing DJs between the apoptotic cell and neighboring non-dying cells remain intact even during the formation of de novo DJs between non-dying cells, suggesting that the neighboring cells possess two DJs in the middle of apoptotic cell extrusion. We further found that an actomyosin cable formed in the vicinity of DJs upon apoptosis, and subsequently deviated from DJs during its constriction. Interestingly, the departure of the actomyosin cable from DJs coincided with the timing when DJs lost their straightness, suggesting a release of junctional tension at DJs, and a mechanical coupling between DJs and actomyosin contractility. The depletion of desmoplakin, which links desmosomes and intermediate filaments, resulted in defective apical contraction and an inability to form de novo DJs, leading to a failure of apoptotic cell extrusion. Our study provides a framework to explain how desmosomes play pivotal roles in maintaining epithelial sheet integrity during apoptotic cell extrusion.

scholarly journals CELL SEGMENTATION WITH RANDOM FERNS AND GRAPH-CUTS

2016 ◽  
Author(s):  
Arnaud Browet ◽  
Christophe De Vleeschouwer ◽  
Laurent Jacques ◽  
Navrita Mathiah ◽  
Bechara Saykali ◽  
...  
Keyword(s):  
Image Segmentation ◽  
Energy Minimization ◽  
Imaging Techniques ◽  
Graph Cuts ◽  
Live Imaging ◽  
Cell Segmentation ◽  
Imaging Data ◽  
Cellular Mechanisms ◽  
Segmentation Framework ◽  
Two Stages

The progress in imaging techniques have allowed the study of various aspect of cellular mechanisms. To isolate individual cells in live imaging data, we introduce an elegant image segmentation framework that effectively extracts cell boundaries, even in the presence of poor edge details. Our approach works in two stages. First, we estimate pixel interior/border/exterior class probabilities using random ferns. Then, we use an energy minimization framework to compute boundaries whose localization is compliant with the pixel class probabilities. We validate our approach on a manually annotated dataset.

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