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 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 Functional Redundancy of the B9 Proteins and Nephrocystins in Caenorhabditis elegans Ciliogenesis

2008 ◽  
Vol 19 (5) ◽  
pp. 2154-2168 ◽  
Author(s):  
Corey L. Williams ◽  
Marlene E. Winkelbauer ◽  
Jenny C. Schafer ◽  
Edward J. Michaud ◽  
Bradley K. Yoder
Keyword(s):  
Caenorhabditis Elegans ◽  
Joubert Syndrome ◽  
Cystic Kidney ◽  
Basal Bodies ◽  
The Novel ◽  
C Elegans ◽  
Human Genes ◽  
Cilia Formation ◽  
Strong Candidate ◽  
Candidate Loci

Meckel-Gruber syndrome (MKS), nephronophthisis (NPHP), and Joubert syndrome (JBTS) are a group of heterogeneous cystic kidney disorders with partially overlapping loci. Many of the proteins associated with these diseases interact and localize to cilia and/or basal bodies. One of these proteins is MKS1, which is disrupted in some MKS patients and contains a B9 motif of unknown function that is found in two other mammalian proteins, B9D2 and B9D1. Caenorhabditis elegans also has three B9 proteins: XBX-7 (MKS1), TZA-1 (B9D2), and TZA-2 (B9D1). Herein, we report that the C. elegans B9 proteins form a complex that localizes to the base of cilia. Mutations in the B9 genes do not overtly affect cilia formation unless they are in combination with a mutation in nph-1 or nph-4, the homologues of human genes (NPHP1 and NPHP4, respectively) that are mutated in some NPHP patients. Our data indicate that the B9 proteins function redundantly with the nephrocystins to regulate the formation and/or maintenance of cilia and dendrites in the amphid and phasmid ciliated sensory neurons. Together, these data suggest that the human homologues of the novel B9 genes B9D2 and B9D1 will be strong candidate loci for pathologies in human MKS, NPHP, and JBTS.

scholarly journals The novel metallothionein genes of Caenorhabditis elegans. Structural organization and inducible, cell-specific expression.

1993 ◽  
Vol 268 (4) ◽  
pp. 2554-2564
Author(s):  
J.H. Freedman ◽  
L.W. Slice ◽  
D. Dixon ◽  
A. Fire ◽  
C.S. Rubin
Keyword(s):  
Caenorhabditis Elegans ◽  
Structural Organization ◽  
The Novel ◽  
Specific Expression

CED-2/CrkII and CED-10/Rac control phagocytosis and cell migration in Caenorhabditis elegans

2000 ◽  
Vol 2 (3) ◽  
pp. 131-136 ◽  
Author(s):  
Peter W. Reddien ◽  
H. Robert Horvitz
Keyword(s):  
Cell Migration ◽  
Caenorhabditis Elegans

A normally attractive cell interaction is repulsive in two C. elegans mesodermal cell migration mutants

Development ◽  
1991 ◽  
Vol 113 (3) ◽  
pp. 797-803 ◽  
Author(s):  
M.J. Stern ◽  
H.R. Horvitz
Keyword(s):  
Cell Migration ◽  
Caenorhabditis Elegans ◽  
Premature Termination ◽  
Cell Interaction ◽  
Egg Laying ◽  
Wild Type ◽  
Mesodermal Cell ◽  
C Elegans ◽  
Somatic Gonad ◽  
Sex Myoblasts

In wild-type Caenorhabditis elegans hermaphrodites, two bilaterally symmetric sex myoblasts (SMs) migrate anteriorly to flank the precise center of the gonad, where they divide to generate the muscles required for egg laying (J. E. Sulston and H. R. Horvitz (1977) Devl Biol. 56, 110–156). Although this migration is largely independent of the gonad, a signal from the gonad attracts the SMs to their precise final positions (J. H. Thomas, M. J. Stern and H. R. Horvitz (1990) Cell 62, 1041–1052). Here we show that mutations in either of two genes, egl-15 and egl-17, cause the premature termination of the migrations of the SMs. This incomplete migration is caused by the repulsion of the SMs by the same cells in the somatic gonad that are the source of the attractive signal in wild-type animals.

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
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