scholarly journals Random versus directionally persistent cell migration

2009 ◽  
Vol 10 (8) ◽  
pp. 538-549 ◽  
Author(s):  
Ryan J. Petrie ◽  
Andrew D. Doyle ◽  
Kenneth M. Yamada
Keyword(s):  
Cell Migration ◽  
Persistent Cell

scholarly journals αvβ3 and α5β1 integrin recycling pathways dictate downstream Rho kinase signaling to regulate persistent cell migration

2007 ◽  
Vol 177 (3) ◽  
pp. 515-525 ◽  
Author(s):  
Dominic P. White ◽  
Patrick T. Caswell ◽  
Jim C. Norman
Keyword(s):  
Cell Migration ◽  
Rho Kinase ◽  
Cell Movement ◽  
Αvβ3 Integrin ◽  
Protein Kinase D1 ◽  
Fibroblast Migration ◽  
Short Loop ◽  
Cell Front ◽  
Α5β1 Integrin ◽  
Persistent Cell

Accumulating evidence suggests that integrin recycling regulates cell migration. However, the lack of reagents to selectively target the trafficking of individual heterodimers, as opposed to endocytic transport as a whole, has made it difficult to define the contribution made by particular recycling pathways to directional cell movement. We show that autophosphorylation of protein kinase D1 (PKD1) at Ser916 is necessary for its association with αvβ3 integrin. Expression of PKD1916A or the use of mutants of β3 that do not bind to PKD1 selectively inhibits short-loop, Rab4-dependent recycling of αvβ3, and this suppresses the persistence of fibroblast migration. However, we report that short-loop recycling does not directly contribute to fibroblast migration by moving αvβ3 to the cell front, but by antagonizing α5β1 recycling, which, in turn, influences the cell's decision to migrate with persistence or to move randomly.

scholarly journals α4β1-Integrin regulates directionally persistent cell migration in response to shear flow stimulation

2008 ◽  
Vol 295 (1) ◽  
pp. C151-C159 ◽  
Author(s):  
Dustin A. Dikeman ◽  
Leslie A. Rivera Rosado ◽  
Troy A. Horn ◽  
Christina S. Alves ◽  
Konstantinos Konstantopoulos ◽  
...  
Keyword(s):  
Cell Migration ◽  
Shear Flow ◽  
Complex Mechanism ◽  
Double Mutation ◽  
Trailing Edges ◽  
Flow Stimulation ◽  
Necessary And Sufficient ◽  
Persistent Cell ◽  
Insight Into

α4β1-Integrin plays a pivotal role in cell migration in vivo. This integrin has been shown to regulate the front-back polarity of migrating cells via localized inhibition of α4-integrin/paxillin binding by phosphorylation at the α4-integrin cytoplasmic tail. Here, we demonstrate that α4β1-integrin regulates directionally persistent cell migration via a more complex mechanism in which α4-integrin phosphorylation and paxillin binding act via both cooperative and independent pathways. We show that, in response to shear flow, α4β1-integrin binding to the CS-1 region of fibronectin was necessary and sufficient to promote directionally persistent cell migration when this integrin was ectopically expressed in CHO cells. Under shear flow, the α4β1-integrin-expressing cells formed a fan shape with broad lamellipodia at the front and retracted trailing edges at the back. This “fanning” activity was enhanced by disrupting paxillin binding alone and inhibited by disrupting phosphorylation alone or together with disrupting paxillin binding. Notably, the phosphorylation-disrupting mutation and the double mutation resulted in the formation of long trailing tails, suggesting that α4-integrin phosphorylation is required for trailing edge retraction/detachment independent of paxillin binding. Furthermore, the stable polarity and directional persistence of shear flow-stimulated cells were perturbed by the double mutation but not the single mutations alone, indicating that paxillin binding and α4-integrin phosphorylation can facilitate directionally persistent cell migration in an independent and compensatory manner. These findings provide a new insight into the mechanism by which integrins regulate directionally persistent cell migration.

Persistent cell migration emerges from a coupling between protrusion dynamics and polarized trafficking

2021 ◽  
Author(s):  
Kotryna Vaidžiulytė ◽  
Anne-Sophie Macé ◽  
Aude Battistella ◽  
William Beng ◽  
Kristine Schauer ◽  
...  
Keyword(s):  
Cell Migration ◽  
Live Cell Imaging ◽  
Cell Movement ◽  
Intrinsic Activity ◽  
Internal Cell ◽  
Polarized Trafficking ◽  
Cell Organization ◽  
Quantitative Properties ◽  
Long Timescales ◽  
Persistent Cell

AbstractMigrating cells present a variety of paths, from random to highly directional ones. While random movement can be explained by basal intrinsic activity, persistent movement requires stable polarization. Here, we quantitatively address emergence of persistent migration in RPE1 cells over long timescales. By live-cell imaging and dynamic micropatterning, we demonstrate that the Nucleus-Golgi axis aligns with direction of migration leading to efficient cell movement. We show that polarized trafficking is directed towards protrusions with a 20 min delay, and that migration becomes random after disrupting internal cell organization. Eventually, we prove that localized optogenetic Cdc42 activation orients the Nucleus-Golgi axis. Our work suggests that polarized trafficking stabilizes the protrusive activity of the cell, while protrusive activity orients this polarity axis, leading to persistent cell migration. Using a minimal physical model, we show that this feedback is sufficient to recapitulate the quantitative properties of cell migration in the timescale of hours.

scholarly journals Phosphorylation of WAVE2 by MAP kinases regulates persistent cell migration and polarity

2007 ◽  
Vol 120 (23) ◽  
pp. 4144-4154 ◽  
Author(s):  
C. M. Danson ◽  
S. M. Pocha ◽  
G. B. Bloomberg ◽  
G. O. Cory
Keyword(s):  
Cell Migration ◽  
Map Kinases ◽  
Persistent Cell

scholarly journals Feedback-Driven Mechanisms Between Phosphorylated Caveolin-1 and Contractile Actin Assemblies Instruct Persistent Cell Migration

2021 ◽  
Vol 9 ◽  
Author(s):  
Xuemeng Shi ◽  
Zeyu Wen ◽  
Yajun Wang ◽  
Yan-Jun Liu ◽  
Kun Shi ◽  
...  
Keyword(s):  
Cell Migration ◽  
Actin Filaments ◽  
Stress Fibers ◽  
Caveolin 1 ◽  
Contractile Stress ◽  
Active Processes ◽  
Outstanding Question ◽  
Directional Cell Migration ◽  
And Control ◽  
Persistent Cell

The actin cytoskeleton and membrane-associated caveolae contribute to active processes, such as cell morphogenesis and motility. How these two systems interact and control directional cell migration is an outstanding question but remains understudied. Here we identified a negative feedback between contractile actin assemblies and phosphorylated caveolin-1 (CAV-1) in migrating cells. Cytoplasmic CAV-1 vesicles display actin-associated motilities by sliding along actin filaments or/and coupling to do retrograde flow with actomyosin bundles. Inhibition of contractile stress fibers, but not Arp2/3-dependent branched actin filaments, diminished the phosphorylation of CAV-1 on site Tyr14, and resulted in substantially increased size and decreased motility of cytoplasmic CAV-1 vesicles. Reciprocally, both the CAV-1 phospho-deficient mutation on site Tyr14 and CAV-1 knockout resulted in dramatic AMPK phosphorylation, further causing reduced active level of RhoA-myosin II and increased active level of Rac1-PAK1-Cofilin, consequently led to disordered contractile stress fibers and prominent lamellipodia. As a result, cells displayed depolarized morphology and compromised directional migration. Collectively, we propose a model in which feedback-driven regulation between actin and CAV-1 instructs persistent cell migration.

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