Genes That Control Cell Migration during Mouse Development

Cell Motility ◽  
2004 ◽  
pp. 317-330 ◽  
Author(s):  
Carmen Birchmeier
Keyword(s):  
Cell Migration ◽  
Control Cell ◽  
Mouse Development

scholarly journals Rudhira/BCAS3 couples microtubules and intermediate filaments to promote cell migration for angiogenic remodeling

2019 ◽  
Vol 30 (12) ◽  
pp. 1437-1450 ◽  
Author(s):  
Divyesh Joshi ◽  
Maneesha S. Inamdar
Keyword(s):  
Cell Migration ◽  
Intermediate Filaments ◽  
Cross Talk ◽  
Control Cell ◽  
The Novel ◽  
Mouse Development ◽  
Cytoskeleton Organization ◽  
Sprouting Angiogenesis ◽  
Promote Cell Migration ◽  
Necessary And Sufficient

Blood vessel formation requires endothelial cell (EC) migration that depends on dynamic remodeling of the cytoskeleton. Rudhira/Breast Carcinoma Amplified Sequence 3 (BCAS3) is a cytoskeletal protein essential for EC migration and sprouting angiogenesis during mouse development and is implicated in metastatic disease. Here, we report that Rudhira mediates cytoskeleton organization and dynamics during EC migration. Rudhira binds to both microtubules (MTs) and vimentin intermediate filaments (IFs) and stabilizes MTs. Rudhira depletion impairs cytoskeletal cross-talk, MT stability, and hence focal adhesion disassembly. The BCAS3 domain of Rudhira is necessary and sufficient for MT-IF cross-linking and cell migration. Pharmacologically restoring MT stability rescues gross cytoskeleton organization and angiogenic sprouting in Rudhira-depleted cells. Our study identifies the novel and essential role of Rudhira in cytoskeletal cross-talk and assigns function to the conserved BCAS3 domain. Targeting Rudhira could allow tissue-restricted cytoskeleton modulation to control cell migration and angiogenesis in development and disease.

scholarly journals Rudhira/BCAS3 couples microtubules and intermediate filaments to promote cell migration for angiogenic remodeling

2018 ◽  
Author(s):  
Divyesh Joshi ◽  
Maneesha S. Inamdar
Keyword(s):  
Cell Migration ◽  
Intermediate Filaments ◽  
Control Cell ◽  
The Novel ◽  
Mouse Development ◽  
Cytoskeleton Organization ◽  
Sprouting Angiogenesis ◽  
Microtubule Stability ◽  
Promote Cell Migration ◽  
Necessary And Sufficient

AbstractBlood vessel formation requires endothelial cell (EC) migration that depends on dynamic remodeling of the cytoskeleton. Rudhira/Breast Carcinoma Amplified Sequence 3 (BCAS3) is a cytoskeletal protein essential for EC migration and sprouting angiogenesis during mouse development and implicated in metastatic disease. Here, we report that Rudhira mediates cytoskeleton organization and dynamics during EC migration. Rudhira binds to both microtubules and Vimentin intermediate filaments (IFs) and stabilizes microtubules. Rudhira depletion impairs cytoskeletal crosstalk, microtubule stability and hence focal adhesion disassembly. The BCAS3 domain of Rudhira is necessary and sufficient for microtubule-IF crosslinking and cell migration. Pharmacologically restoring microtubule stability rescues gross cytoskeleton organization and angiogenic sprouting in Rudhira depleted cells. Our study identifies the novel and essential role of Rudhira in cytoskeletal crosstalk and assigns function to the conserved BCAS3 domain. Targeting Rudhira could allow tissue-restricted cytoskeleton modulation to control cell migration and angiogenesis in development and disease.

scholarly journals The Novel Secreted Factor MIG-18 Acts with MIG-17/ADAMTS to Control Cell Migration in Caenorhabditis elegans

Genetics ◽  
2013 ◽  
Vol 196 (2) ◽  
pp. 471-479 ◽  
Author(s):  
Hon-Song Kim ◽  
Yuko Kitano ◽  
Masataka Mori ◽  
Tomomi Takano ◽  
Thomas Edward Harbaugh ◽  
...  
Keyword(s):  
Cell Migration ◽  
Caenorhabditis Elegans ◽  
Control Cell ◽  
The Novel

scholarly journals Immersion technique for the preparation of protein gradients on Collagen Type I membranes to control cell migration

2019 ◽  
Vol 4 (1-2) ◽  
pp. 43-49 ◽  
Author(s):  
Steffen Berger ◽  
Jan Kiebist ◽  
Elisabeth Pötschke ◽  
Katrin Salchert
Keyword(s):  
Cell Migration ◽  
Collagen Type ◽  
Control Cell ◽  
Collagen Type I ◽  
Type I ◽  
Immersion Technique ◽  
Protein Gradients

scholarly journals Phosphorylation of ACAP1 by Akt Regulates the Stimulation-Dependent Recycling of Integrin β1 to Control Cell Migration

2005 ◽  
Vol 9 (5) ◽  
pp. 663-673 ◽  
Author(s):  
Jian Li ◽  
Bryan A. Ballif ◽  
Aimee M. Powelka ◽  
Jun Dai ◽  
Steven P. Gygi ◽  
...  
Keyword(s):  
Cell Migration ◽  
Control Cell ◽  
Integrin Β1

scholarly journals A family affair: A Ral-exocyst-centered network links Ras, Rac, Rho signaling to control cell migration

Small GTPases ◽  
2017 ◽  
Vol 10 (5) ◽  
pp. 323-330 ◽  
Author(s):  
Giulia Zago ◽  
Marco Biondini ◽  
Jacques Camonis ◽  
Maria Carla Parrini
Keyword(s):  
Cell Migration ◽  
Control Cell ◽  
Network Links

scholarly journals Synthetic dysmobility screen unveils an integrated STK40-YAP-MAPK system driving cell migration

2021 ◽  
Author(s):  
Ling-Yea Yu ◽  
Ting-Jen Tseng ◽  
Hsuan-Chao Lin ◽  
Ting-Xuan Lu ◽  
Chia-Jung Tsai ◽  
...  
Keyword(s):  
Cell Migration ◽  
Focal Adhesion ◽  
Synthetic Lethality ◽  
Control Cell ◽  
Mitogen Activated Protein Kinase ◽  
Serine Threonine Kinase ◽  
Threonine Kinase ◽  
Mitogen Activated Protein ◽  
Novel Strategy ◽  
Migration Of Cells

AbstractIntegrating signals is essential for cell survival, leading to the concept of synthetic lethality. However, how signaling is integrated to control cell migration remains unclear. By conducting a “two-hit” screen, we revealed the synergistic reduction of cell migration when serine-threonine kinase 40 (STK40) and mitogen-activated protein kinase (MAPK) were simultaneously suppressed. Single-cell analyses showed that STK40 knockdown reduced cell motility and coordination by strengthening focal adhesion (FA) complexes. Furthermore, STK40 knockdown reduced translocation of yes-associated protein (YAP) into the nucleus, while MAPK inhibition further weakened YAP activities in the nucleus to disturb FA remodeling. Altogether, we unveiled an integrated STK40-YAP-MAPK system regulating cell migration, and introduced “synthetic dysmobility” as a novel strategy to collaboratively control cell migration.One Sentence SummaryBlocking collaborative pathways within the integrated signaling network synergistically disrupts the migration of cells.

scholarly journals Distinct phospho-forms of cortactin differentially regulate actin polymerization and focal adhesions

2008 ◽  
Vol 295 (5) ◽  
pp. C1113-C1122 ◽  
Author(s):  
Anne E. Kruchten ◽  
Eugene W. Krueger ◽  
Yu Wang ◽  
Mark A. McNiven
Keyword(s):  
Cell Migration ◽  
Focal Adhesion ◽  
Actin Polymerization ◽  
Control Cell ◽  
Focal Adhesions ◽  
Serine Phosphorylation ◽  
Actin Binding ◽  
Actin Assembly

Cortactin is an actin-binding protein that is overexpressed in many cancers and is a substrate for both tyrosine and serine/threonine kinases. Tyrosine phosphorylation of cortactin has been observed to increase cell motility and invasion in vivo, although it has been reported to have both positive and negative effects on actin polymerization in vitro. In contrast, serine phosphorylation of cortactin has been shown to stimulate actin assembly in vitro. Currently, the effects of cortactin serine phosphorylation on cell migration are unclear, and furthermore, how the distinct phospho-forms of cortactin may differentially contribute to cell migration has not been directly compared. Therefore, we tested the effects of different tyrosine and serine phospho-mutants of cortactin on lamellipodial protrusion, actin assembly within cells, and focal adhesion dynamics. Interestingly, while expression of either tyrosine or serine phospho-mimetic cortactin mutants resulted in increased lamellipodial protrusion and cell migration, these effects appeared to be via distinct processes. Cortactin mutants mimicking serine phosphorylation appeared to predominantly affect actin polymerization, whereas mutation of cortactin tyrosine residues resulted in alterations in focal adhesion turnover. Thus these findings provide novel insights into how distinct phospho-forms of cortactin may differentially contribute to actin and focal adhesion dynamics to control cell migration.

scholarly journals Ras regulates kinesin 13 family members to control cell migration pathways in transformed human bronchial epithelial cells

Oncogene ◽  
2013 ◽  
Vol 33 (47) ◽  
pp. 5457-5466 ◽  
Author(s):  
E Zaganjor ◽  
J K Osborne ◽  
L M Weil ◽  
L A Diaz-Martinez ◽  
J X Gonzales ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
Control Cell ◽  
Family Members ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Migration Pathways
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