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

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

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.

Control of cell migration during Caenorhabditis elegans development

1999 ◽  
Vol 11 (5) ◽  
pp. 608-613 ◽  
Author(s):  
Robert Blelloch ◽  
Craig Newman ◽  
Judith Kimble
Keyword(s):  
Cell Migration ◽  
Caenorhabditis Elegans

scholarly journals Distinct Rac Activation Pathways Control Caenorhabditis elegans Cell Migration and Axon Outgrowth

2002 ◽  
Vol 250 (1) ◽  
pp. 145-155 ◽  
Author(s):  
Yi-Chun Wu ◽  
Ting-Wen Cheng ◽  
Ming-Chia Lee ◽  
Nei-Ying Weng
Keyword(s):  
Cell Migration ◽  
Caenorhabditis Elegans ◽  
Axon Outgrowth ◽  
Activation Pathways

scholarly journals The Nc1/Endostatin Domain of Caenorhabditis elegans Type Xviii Collagen Affects Cell Migration and Axon Guidance

2001 ◽  
Vol 152 (6) ◽  
pp. 1219-1232 ◽  
Author(s):  
Brian D. Ackley ◽  
Jennifer R. Crew ◽  
Harri Elamaa ◽  
Tania Pihlajaniemi ◽  
Calvin J. Kuo ◽  
...  
Keyword(s):  
Cell Migration ◽  
Caenorhabditis Elegans ◽  
Axon Guidance ◽  
Ectopic Expression ◽  
Basement Membranes ◽  
Protein Isoforms ◽  
Developmentally Regulated ◽  
C Elegans ◽  
Collagen Xviii ◽  
Nc1 Domain

Type XVIII collagen is a homotrimeric basement membrane molecule of unknown function, whose COOH-terminal NC1 domain contains endostatin (ES), a potent antiangiogenic agent. The Caenorhabditis elegans collagen XVIII homologue, cle-1, encodes three developmentally regulated protein isoforms expressed predominantly in neurons. The CLE-1 protein is found in low amounts in all basement membranes but accumulates at high levels in the nervous system. Deletion of the cle-1 NC1 domain results in viable fertile animals that display multiple cell migration and axon guidance defects. Particular defects can be rescued by ectopic expression of the NC1 domain, which is shown to be capable of forming trimers. In contrast, expression of monomeric ES does not rescue but dominantly causes cell and axon migration defects that phenocopy the NC1 deletion, suggesting that ES inhibits the promigratory activity of the NC1 domain. These results indicate that the cle-1 NC1/ES domain regulates cell and axon migrations in C. elegans.

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