scholarly journals The dosage-dependent effect exerted by the NM23-H1/H2 homolog NDK-1 on distal tip cell migration in C. elegans

2017 ◽  
Vol 98 (2) ◽  
pp. 182-189 ◽  
Author(s):  
Zsolt Farkas ◽  
Luca Fancsalszky ◽  
Éva Saskői ◽  
Alexandra Gráf ◽  
Krisztián Tárnok ◽  
...  
2010 ◽  
Vol 341 (1) ◽  
pp. 176-185 ◽  
Author(s):  
Hiba Tannoury ◽  
Varenka Rodriguez ◽  
Ismar Kovacevic ◽  
Mouna Ibourk ◽  
Myeongwoo Lee ◽  
...  
Keyword(s):  
Tip Cell ◽  

2010 ◽  
Vol 344 (2) ◽  
pp. e1
Author(s):  
Hiba Tannoury ◽  
Varenka Rodriguez ◽  
Ismar Kovacevic ◽  
Mouna Ibourk ◽  
Myeongwoo Lee ◽  
...  
Keyword(s):  
Tip Cell ◽  

2006 ◽  
Vol 289 (1) ◽  
pp. 229-242 ◽  
Author(s):  
Anna Y. Zinovyeva ◽  
Serena M. Graham ◽  
Veronica J. Cloud ◽  
Wayne C. Forrester

Development ◽  
2001 ◽  
Vol 128 (22) ◽  
pp. 4475-4488 ◽  
Author(s):  
Erik A. Lundquist ◽  
Peter W. Reddien ◽  
Erika Hartwieg ◽  
H. Robert Horvitz ◽  
Cornelia I. Bargmann

The Caenorhabditis elegans genome contains three rac-like genes, ced-10, mig-2, and rac-2. We report that ced-10, mig-2 and rac-2 act redundantly in axon pathfinding: inactivating one gene had little effect, but inactivating two or more genes perturbed both axon outgrowth and guidance. mig-2 and ced-10 also have redundant functions in some cell migrations. By contrast, ced-10 is uniquely required for cell-corpse phagocytosis, and mig-2 and rac-2 have only subtle roles in this process. Rac activators are also used differentially. The UNC-73 Trio Rac GTP exchange factor affected all Rac pathways in axon pathfinding and cell migration but did not affect cell-corpse phagocytosis. CED-5 DOCK180, which acts with CED-10 Rac in cell-corpse phagocytosis, acted with MIG-2 but not CED-10 in axon pathfinding. Thus, distinct regulatory proteins modulate Rac activation and function in different developmental processes.


2008 ◽  
Vol 105 (52) ◽  
pp. 20804-20809 ◽  
Author(s):  
Y. Kubota ◽  
K. Ohkura ◽  
K. K. Tamai ◽  
K. Nagata ◽  
K. Nishiwaki

Development ◽  
1994 ◽  
Vol 120 (10) ◽  
pp. 2901-2911 ◽  
Author(s):  
S.L. Crittenden ◽  
E.R. Troemel ◽  
T.C. Evans ◽  
J. Kimble

In C. elegans, germline mitosis depends on induction by the somatic distal tip cell (DTC) and on activity of the glp-1 gene. Using antibodies to GLP-1 protein, we have examined GLP-1 on western blots and by immunocytochemistry. GLP-1 is tightly associated with membranes of mitotic germline cells, supporting its identification as an integral membrane protein. Furthermore, GLP-1 is localized within the germ line to the mitotic region, consistent with the model that GLP-1 acts as a membrane receptor for the distal tip cell signal. Unexpectedly, GLP-1 and the zone of mitosis extend further than the DTC processes. We present three models by which the DTC may influence GLP-1 activity and thereby determine the zone of mitosis. The spatial restriction of GLP-1 appears to be controlled at the translational level in hermaphrodites. We suggest that down-regulation of GLP-1 may be required to effect the transition from mitosis into meiosis.


Development ◽  
1991 ◽  
Vol 113 (3) ◽  
pp. 797-803 ◽  
Author(s):  
M.J. Stern ◽  
H.R. Horvitz

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.


2009 ◽  
Vol 185 (1) ◽  
pp. 77-85 ◽  
Author(s):  
Guangshuo Ou ◽  
Ronald D. Vale

Metazoan cell movement has been studied extensively in vitro, but cell migration in living animals is much less well understood. In this report, we have studied the Caenorhabditis elegans Q neuroblast lineage during larval development, developing live animal imaging methods for following neuroblast migration with single cell resolution. We find that each of the Q descendants migrates at different speeds and for distinct distances. By quantitative green fluorescent protein imaging, we find that Q descendants that migrate faster and longer than their sisters up-regulate protein levels of MIG-2, a Rho family guanosine triphosphatase, and/or down-regulate INA-1, an integrin α subunit, during migration. We also show that Q neuroblasts bearing mutations in either MIG-2 or INA-1 migrate at reduced speeds. The migration defect of the mig-2 mutants, but not ina-1, appears to result from a lack of persistent polarization in the direction of cell migration. Thus, MIG-2 and INA-1 function distinctly to control Q neuroblast migration in living C. elegans.


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