scholarly journals Analyses of Actin Dynamics, Clutch Coupling and Traction Force for Growth Cone Advance

10.3791/63227 ◽  
2021 ◽  
Author(s):  
Takunori Minegishi ◽  
Ryosuke Fujikawa ◽  
Ria Fajarwati Kastian ◽  
Yuichi Sakumura ◽  
Naoyuki Inagaki
Keyword(s):  
Growth Cone ◽  
Traction Force ◽  
Actin Dynamics

scholarly journals Actin dynamics in growth cone motility and navigation

2013 ◽  
Vol 129 (2) ◽  
pp. 221-234 ◽  
Author(s):  
Timothy M. Gomez ◽  
Paul C. Letourneau
Keyword(s):  
Growth Cone ◽  
Actin Dynamics

scholarly journals Grip and slip of L1-CAM on adhesive substrates direct growth cone haptotaxis

2018 ◽  
Vol 115 (11) ◽  
pp. 2764-2769 ◽  
Author(s):  
Kouki Abe ◽  
Hiroko Katsuno ◽  
Michinori Toriyama ◽  
Kentarou Baba ◽  
Tomoyuki Mori ◽  
...  
Keyword(s):  
Cell Migration ◽  
Growth Cone ◽  
Cell Adhesion Molecule ◽  
Chemical Cues ◽  
Traction Force ◽  
Human Patient ◽  
Direct Growth ◽  
Direct Cell ◽  
Conventional Cell ◽  
Directional Cell Migration

Chemical cues presented on the adhesive substrate direct cell migration, a process termed haptotaxis. To migrate, cells must generate traction forces upon the substrate. However, how cells probe substrate-bound cues and generate directional forces for migration remains unclear. Here, we show that the cell adhesion molecule (CAM) L1-CAM is involved in laminin-induced haptotaxis of axonal growth cones. L1-CAM underwent grip and slip on the substrate. The ratio of the grip state was higher on laminin than on the control substrate polylysine; this was accompanied by an increase in the traction force upon laminin. Our data suggest that the directional force for laminin-induced growth cone haptotaxis is generated by the grip and slip of L1-CAM on the substrates, which occur asymmetrically under the growth cone. This mechanism is distinct from the conventional cell signaling models for directional cell migration. We further show that this mechanism is disrupted in a human patient with L1-CAM syndrome, suffering corpus callosum agenesis and corticospinal tract hypoplasia.

scholarly journals Transmission of growth cone traction force through apCAM–cytoskeletal linkages is regulated by Src family tyrosine kinase activity

2001 ◽  
Vol 155 (3) ◽  
pp. 427-438 ◽  
Author(s):  
Daniel M. Suter ◽  
Paul Forscher
Keyword(s):  
Tyrosine Kinase ◽  
Growth Cone ◽  
Kinase Activity ◽  
Kinase Inhibitors ◽  
Traction Force ◽  
Tyrosine Kinase Activity ◽  
Cellular Mechanisms ◽  
Traction Forces ◽  
Kinase Activation ◽  
Neuronal Growth Cone

Tyrosine kinase activity is known to be important in neuronal growth cone guidance. However, underlying cellular mechanisms are largely unclear. Here, we report how Src family tyrosine kinase activity controls apCAM-mediated growth cone steering by regulating the transmission of traction forces through receptor–cytoskeletal linkages. Increased levels of tyrosine phosphorylation were detected at sites where beads coated with apCAM ligands were physically restrained to induce growth cone steering, but not at unrestrained bead binding sites. Interestingly, the rate and level of phosphotyrosine buildup near restrained beads were decreased by the myosin inhibitor 2,3-butanedione-2-monoxime, suggesting that tension promotes tyrosine kinase activation. While not affecting retrograde F-actin flow rates, genistein and the Src family selective tyrosine kinase inhibitors PP1 and PP2 strongly reduced the growth cone's ability to apply traction forces through apCAM–cytoskeletal linkages, assessed using the restrained bead interaction assay. Furthermore, increased levels of an activated Src family kinase were detected at restrained bead sites during growth cone steering events. Our results suggest a mechanism by which growth cones select pathways by sampling both the molecular nature of the substrate and its ability to withstand the application of traction forces.

scholarly journals BMP gradients steer nerve growth cones by a balancing act of LIM kinase and Slingshot phosphatase on ADF/cofilin

2007 ◽  
Vol 178 (1) ◽  
pp. 107-119 ◽  
Author(s):  
Zhexing Wen ◽  
Liang Han ◽  
James R. Bamburg ◽  
Sangwoo Shim ◽  
Guo-li Ming ◽  
...  
Keyword(s):  
Growth Cone ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Growth Cones ◽  
Actin Dynamics ◽  
Lim Kinase ◽  
Nerve Growth ◽  
Nerve Growth Cones ◽  
Transient Receptor ◽  
Calcineurin Phosphatase

Bone morphogenic proteins (BMPs) are involved in axon pathfinding, but how they guide growth cones remains elusive. In this study, we report that a BMP7 gradient elicits bidirectional turning responses from nerve growth cones by acting through LIM kinase (LIMK) and Slingshot (SSH) phosphatase to regulate actin-depolymerizing factor (ADF)/cofilin-mediated actin dynamics. Xenopus laevis growth cones from 4–8-h cultured neurons are attracted to BMP7 gradients but become repelled by BMP7 after overnight culture. The attraction and repulsion are mediated by LIMK and SSH, respectively, which oppositely regulate the phosphorylation-dependent asymmetric activity of ADF/cofilin to control the actin dynamics and growth cone steering. The attraction to repulsion switching requires the expression of a transient receptor potential (TRP) channel TRPC1 and involves Ca2+ signaling through calcineurin phosphatase for SSH activation and growth cone repulsion. Together, we show that spatial regulation of ADF/cofilin activity controls the directional responses of the growth cone to BMP7, and Ca2+ influx through TRPC tilts the LIMK-SSH balance toward SSH-mediated repulsion.

scholarly journals Growth cone behavior and production of traction force.

1990 ◽  
Vol 111 (5) ◽  
pp. 1949-1957 ◽  
Author(s):  
S R Heidemann ◽  
P Lamoureux ◽  
R E Buxbaum
Keyword(s):  
Growth Cone ◽  
Contractile Activity ◽  
Glass Fibers ◽  
Force Production ◽  
Traction Force ◽  
Dorsal Surface ◽  
Growth Cones ◽  
Retrograde Flow ◽  
Cortical Actin ◽  
Over The Top

The growth cone must push its substrate rearward via some traction force in order to propel itself forward. To determine which growth cone behaviors produce traction force, we observed chick sensory growth cones under conditions in which force production was accommodated by movement of obstacles in the environment, namely, neurites of other sensory neurons or glass fibers. The movements of these obstacles occurred via three, different, stereotyped growth cone behaviors: (a) filopodial contractions, (b) smooth rearward movement on the dorsal surface of the growth cone, and (c) interactions with ruffling lamellipodia. More than 70% of the obstacle movements were caused by filopodial contractions in which the obstacle attached at the extreme distal end of a filopodium and moved only as the filopodium changed its extension. Filopodial contractions were characterized by frequent changes of obstacle velocity and direction. Contraction of a single filopodium is estimated to exert 50-90 microdyn of force, which can account for the pull exerted by chick sensory growth cones. Importantly, all five cases of growth cones growing over the top of obstacle neurites (i.e., geometry that mimics the usual growth cone/substrate interaction), were of the filopodial contraction type. Some 25% of obstacle movements occurred by a smooth backward movement along the top surface of growth cones. Both the appearance and rate of movements were similar to that reported for retrograde flow of cortical actin near the dorsal growth cone surface. Although these retrograde flow movements also exerted enough force to account for growth cone pulling, we did not observe such movements on ventral growth cone surfaces. Occasionally obstacles were moved by interaction with ruffling lamellipodia. However, we obtained no evidence for attachment of the obstacles to ruffling lamellipodia or for directed obstacle movements by this mechanism. These data suggest that chick sensory growth cones move forward by contractile activity of filopodia, i.e., isometric contraction on a rigid substrate. Our data argue against retrograde flow of actin producing traction force.

scholarly journals Adhesive L1CAM-Robo Signaling Aligns Growth Cone F-Actin Dynamics to Promote Axon-Dendrite Fasciculation in C. elegans

2019 ◽  
Vol 49 (3) ◽  
pp. 490-491 ◽  
Author(s):  
Chun-Hao Chen ◽  
Hao-Wei Hsu ◽  
Yun-Hsuan Chang ◽  
Chun-Liang Pan
Keyword(s):  
Growth Cone ◽  
Actin Dynamics ◽  
C Elegans

scholarly journals The Role of Arp2/3 in Growth Cone Actin Dynamics and Guidance Is Substrate Dependent

2014 ◽  
Vol 34 (17) ◽  
pp. 5895-5908 ◽  
Author(s):  
J. E. San Miguel-Ruiz ◽  
P. C. Letourneau
Keyword(s):  
Growth Cone ◽  
Actin Dynamics

Subcellular localization of myosin V in nerve growth cones and outgrowth from dilute-lethal neurons

1997 ◽  
Vol 110 (4) ◽  
pp. 439-449 ◽  
Author(s):  
L.L. Evans ◽  
J. Hammer ◽  
P.C. Bridgman
Keyword(s):  
Growth Cone ◽  
Actin Filaments ◽  
Traction Force ◽  
Growth Cones ◽  
Neuronal Function ◽  
Neuronal Structure ◽  
Myosin V ◽  
Cytoskeletal Organization ◽  
Cervical Ganglion ◽  
Nerve Growth Cones

Myosin V-null mice (dilute-lethal mutants) exhibit apparent neurological defects that worsen from birth until death in the third postnatal week. Although myosin V is enriched in brain, the neuronal function of myosin V is unclear and the underlying cause of the neurological defects in these mice is unknown. To aide in understanding myosin V function, we examined the distribution of myosin V in the rodent superior cervical ganglion (SCG) growth cone, a well characterized neuronal structure in which myosin V is concentrated. Using affinity purified, myosin V-specific antibodies in immunofluorescence and immunoelectron microscopy, we observed that myosin V is concentrated in organelle-rich regions of the growth cone. Myosin V is present on a distinct population of small (50–100 nm) organelles, and on actin filaments and the plasma membrane. Myosin V-associated organelles are present on both microtubules and actin filaments. These results indicate that myosin V may be carried as a passenger on organelles that are transported along microtubules, and that these organelles may also be capable of movement along actin filaments. In addition, we found no abnormalities in outgrowth, morphology, or cytoskeletal organization of SCG growth cones from dilute-lethal mice. These results indicate that myosin V is not necessary for the traction force needed for growth cone locomotion, for organization of the actin cytoskeleton, or for filopodial dynamics.

scholarly journals The Level of Substrate Deformation and not Traction Force Regulates Adhesion-Mediated Neuronal Growth Cone Advance

2015 ◽  
Vol 108 (2) ◽  
pp. 305a
Author(s):  
Ahmad I.M. Athamneh ◽  
Alexander X. Cartagena-Rivera ◽  
Arvind Raman ◽  
Daniel M. Suter
Keyword(s):  
Growth Cone ◽  
Traction Force ◽  
Neuronal Growth ◽  
Neuronal Growth Cone
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