scholarly journals The mechanosensitive channel Piezo1 cooperates with Semaphorin to control neural crest migration

Development ◽  
2021 ◽  
Author(s):  
Brenda Canales Coutiño ◽  
Roberto Mayor
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Embryonic Cell ◽  
Extracellular Signals ◽  
Rac1 Activity ◽  
Cytoskeletal Dynamics ◽  
Mechanosensitive Ion Channel ◽  
Neural Crest Migration

Cells are permanently exposed to a multitude of different kind of signals; however how cells respond to simultaneous extracellular signals within a complex in vivo environment is poorly understood. Here, we studied the role of the mechanosensitive ion channel Piezo1 on the migration of the neural crest (NC), a multipotent embryonic cell population. We identify that Piezo1 is required for the migration of Xenopus cephalic NC. We show that loss of Piezo1 promotes focal adhesion turnover and cytoskeletal dynamics by controlling Rac1 activity, leading to increased speed of migration. Moreover, overactivation of Rac1, due to Piezo1 inhibition, counteracts cell migration inhibitory signals by Semaphorins 3A and 3F, generating aberrant neural crest invasion in vivo. Thus, we find that, for directional migration in vivo, neural crest cells require a tight regulation of Rac1, by Semaphorins and Piezo1. We reveal here that a balance between a myriad of signals through Rac1 dictates cell migration in vivo, a mechanism that is likely to be conserved in other cell migration processes.

scholarly journals Ca2+/H+ exchange by acidic organelles regulates cell migration in vivo

2016 ◽  
Vol 212 (7) ◽  
pp. 803-813 ◽  
Author(s):  
Manuela Melchionda ◽  
Jon K. Pittman ◽  
Roberto Mayor ◽  
Sandip Patel
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Cell Matrix ◽  
Physiological Relevance ◽  
Underlying Mechanisms ◽  
Acidic Organelles ◽  
Cell Matrix Adhesion ◽  
Insight Into

Increasing evidence implicates Ca2+ in the control of cell migration. However, the underlying mechanisms are incompletely understood. Acidic Ca2+ stores are fast emerging as signaling centers. But how Ca2+ is taken up by these organelles in metazoans and the physiological relevance for migration is unclear. Here, we identify a vertebrate Ca2+/H+ exchanger (CAX) as part of a widespread family of homologues in animals. CAX is expressed in neural crest cells and required for their migration in vivo. It localizes to acidic organelles, tempers evoked Ca2+ signals, and regulates cell-matrix adhesion during migration. Our data provide new molecular insight into how Ca2+ is handled by acidic organelles and link this to migration, thereby underscoring the role of noncanonical Ca2+ stores in the control of Ca2+-dependent function.

scholarly journals How inhibitory cues can both constrain and promote cell migration

2016 ◽  
Vol 213 (5) ◽  
pp. 505-507 ◽  
Author(s):  
Marianne E. Bronner
Keyword(s):  
Mathematical Modeling ◽  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cells ◽  
Collective Cell Migration ◽  
Promote Cell Migration ◽  
Neural Crest Migration ◽  
Physical Boundary

Collective cell migration is a common feature in both embryogenesis and metastasis. By coupling studies of neural crest migration in vivo and in vitro with mathematical modeling, Szabó et al. (2016, J. Cell Biol., http://dx.doi.org/10.1083/jcb.201602083) demonstrate that the proteoglycan versican forms a physical boundary that constrains neural crest cells to discrete streams, in turn facilitating their migration.

scholarly journals Stretch-induced endogenous electric fields drive neural crest directed collective cell migration in vivo

2021 ◽  
Author(s):  
Fernando Ferreira ◽  
Sofia Moreira ◽  
Elias H Barriga
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Electric Fields ◽  
Embryonic Cell ◽  
Collective Cell Migration ◽  
Convergent Extension ◽  
Topological Features ◽  
Stretch Activated Channels

Directed collective cell migration (dCCM) is essential for morphogenesis. Cell clusters migrate in inherently complex in vivo environments composed of chemical, electrical, mechanical as well as topological features. While these environmental factors have been shown to allow dCCM in vitro, our understanding of dCCM in vivo is mostly limited to chemical guidance. Thus, despite its wide biological relevance, the mechanisms that guide dCCM in vivo remain unclear. To address this, we study endogenous electric fields in relation to the migratory environment of the Xenopus laevis cephalic neural crest, an embryonic cell population that collectively and directionally migrates in vivo. Combining bioelectrical, biomechanical and molecular tools, we show that endogenous electric fields drive neural crest dCCM via electrotaxis in vivo. Moreover, we identify the voltage-sensitive phosphatase 1 (Vsp1) as a key component of the molecular mechanism used by neural crest cells to transduce electric fields into a directional cue. Furthermore, Vsp1 function is specifically required for electrotaxis, being dispensable for cell motility and chemotaxis. Finally, we reveal that endogenous electric fields are mechanoelectrically established. Mechanistically, convergent extension movements of the neural fold generate membrane tension, which in turn opens stretch-activated channels to mobilise the ions required to fuel electric fields. Overall, our results reveal a mechanism of cell guidance, where electrotaxis emerges from the mechanoelectrical and molecular interplay between neighbouring tissues. More broadly, our data contribute to validate the, otherwise understudied, functions of endogenous bioelectrical stimuli in morphogenetic processes.

scholarly journals Connexin43 controls N-cadherin transcription during collective cell migration

2017 ◽  
Author(s):  
Maria Kotini ◽  
Elias H. Barriga ◽  
Jonathan Leslie ◽  
Marc Gentzel ◽  
Alexandra Schambony ◽  
...  
Keyword(s):  
Cell Migration ◽  
Gap Junctions ◽  
Neural Crest ◽  
Cancer Metastasis ◽  
Embryonic Cell ◽  
Collective Cell Migration ◽  
List Type ◽  
Cellular Processes ◽  
Physiological Processes

AbstractConnexins are the primary components of gap junctions, providing direct links between cells in many physiological processes, including cell migration and cancer metastasis. Exactly how cell migration is controlled by gap junctions remains a mystery. To shed light on this, we investigated the role of Connexin43 in collective cell migration during embryo development using the neural crest, an embryonic cell population whose migratory behavior has been likened to cancer invasion. We discovered that Connexin43 is required for contact inhibition of locomotion by directly regulating the transcription of N-cadherin. For this function, the Connexin43 carboxy tail interacts with Basic Transcription Factor 3, which mediates its translocation to the nucleus. Together, they bind to the n-cad promotor regulating n-cad transcription. Thus, we uncover an unexpected, gap junction-independent role for Connexin43 in collective migration that illustrates the possibility that connexins, in general, may be important for a wide variety of cellular processes that we are only beginning to understand.HighlightsCx43 regulates collective directional migration of neural crest cellsCx43 carboxy tail controls cell polarity via n-cad regulationCx43 carboxy tail localises at the nucleus and that depends on BTF3BTF3 and Cx43 carboxy tail directly interact to bind and regulate n-cad promoter activity

scholarly journals GSK3 Controls Migration of the Neural Crest Lineage

2018 ◽  
Author(s):  
Sandra G. Gonzalez Malagon ◽  
Anna M. Lopez Muñoz ◽  
Daniel Doro ◽  
Triòna G. Bolger ◽  
Evon Poon ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Glycogen Synthase ◽  
Neuroblastoma Cells ◽  
Neural Crest Cells ◽  
Anaplastic Lymphoma ◽  
Neural Crest Development ◽  
And Migration ◽  
Neural Crest Migration

AbstractMigration of the neural crest lineage is critical to its physiological function. Mechanisms controlling neural crest migration are comparatively unknown, due to difficulties accessing this cell population in vivo. Here, we uncover novel requirements of glycogen synthase kinase 3 (GSK3) in regulating the neural crest. We demonstrate that GSK3 is tyrosine phosphorylated (pY) in neural crest cells and that this activation depends on anaplastic lymphoma kinase (ALK), a protein associated with neuroblastoma. Consistent with this, neuroblastoma cells with pathologically increased ALK activity express high levels of pY-GSK3 and migration of these cells can be inhibited by GSK3 or ALK blockade. In normal neural crest cells, loss of GSK3 leads to increased pFAK and misregulation of Rac1 and lamellipodin, key regulators of cell migration. Genetic reduction of GSK-3 results in failure of migration. All together, this work identifies a role for GSK3 in cell migration during neural crest development and cancer.

scholarly journals Macropinocytosis-mediated membrane recycling drives neural crest migration by delivering F-actin to the lamellipodium

2020 ◽  
Vol 117 (44) ◽  
pp. 27400-27411 ◽  
Author(s):  
Yuwei Li ◽  
Walter G. Gonzalez ◽  
Andrey Andreev ◽  
Weiyi Tang ◽  
Shashank Gandhi ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Individual Cell ◽  
Lipid Vesicles ◽  
Cell Polarization ◽  
Circular Membrane ◽  
Membrane Recycling ◽  
Membrane Flow ◽  
Neural Crest Migration

Individual cell migration requires front-to-back polarity manifested by lamellipodial extension. At present, it remains debated whether and how membrane motility mediates this cell morphological change. To gain insights into these processes, we perform live imaging and molecular perturbation of migrating chick neural crest cells in vivo. Our results reveal an endocytic loop formed by circular membrane flow and anterograde movement of lipid vesicles, resulting in cell polarization and locomotion. Rather than clathrin-mediated endocytosis, macropinosomes encapsulate F-actin in the cell body, forming vesicles that translocate via microtubules to deliver actin to the anterior. In addition to previously proposed local conversion of actin monomers to polymers, we demonstrate a surprising role for shuttling of F-actin across cells for lamellipodial expansion. Thus, the membrane and cytoskeleton act in concert in distinct subcellular compartments to drive forward cell migration.

scholarly journals Lamellipodin and the Scar/WAVE complex cooperate to promote cell migration in vivo

2013 ◽  
Vol 203 (4) ◽  
pp. 673-689 ◽  
Author(s):  
Ah-Lai Law ◽  
Anne Vehlow ◽  
Maria Kotini ◽  
Lauren Dodgson ◽  
Daniel Soong ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Direct Interaction ◽  
Dependent Manner ◽  
Border Cell ◽  
Promote Cell Migration ◽  
Wave Complex

Cell migration is essential for development, but its deregulation causes metastasis. The Scar/WAVE complex is absolutely required for lamellipodia and is a key effector in cell migration, but its regulation in vivo is enigmatic. Lamellipodin (Lpd) controls lamellipodium formation through an unknown mechanism. Here, we report that Lpd directly binds active Rac, which regulates a direct interaction between Lpd and the Scar/WAVE complex via Abi. Consequently, Lpd controls lamellipodium size, cell migration speed, and persistence via Scar/WAVE in vitro. Moreover, Lpd knockout mice display defective pigmentation because fewer migrating neural crest-derived melanoblasts reach their target during development. Consistently, Lpd regulates mesenchymal neural crest cell migration cell autonomously in Xenopus laevis via the Scar/WAVE complex. Further, Lpd’s Drosophila melanogaster orthologue Pico binds Scar, and both regulate collective epithelial border cell migration. Pico also controls directed cell protrusions of border cell clusters in a Scar-dependent manner. Taken together, Lpd is an essential, evolutionary conserved regulator of the Scar/WAVE complex during cell migration in vivo.

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