scholarly journals A C. elegans Myc-like network cooperates with semaphorin and Wnt signaling pathways to control cell migration

2007 ◽  
Vol 310 (2) ◽  
pp. 226-239 ◽  
Author(s):  
Christopher L. Pickett ◽  
Kevin T. Breen ◽  
Donald E. Ayer
Development ◽  
2001 ◽  
Vol 128 (15) ◽  
pp. 3001-3015 ◽  
Author(s):  
Pamela L. Bradley ◽  
Deborah J. Andrew

During development, directed cell migration is crucial for achieving proper shape and function of organs. One well-studied example is the embryonic development of the larval tracheal system of Drosophila, in which at least four signaling pathways coordinate cell migration to form an elaborate branched network essential for oxygen delivery throughout the larva. FGF signaling is required for guided migration of all tracheal branches, whereas the DPP, EGF receptor, and Wingless/WNT signaling pathways each mediate the formation of specific subsets of branches. Here, we characterize ribbon, which encodes a BTB/POZ-containing protein required for specific tracheal branch migration. In ribbon mutant tracheae, the dorsal trunk fails to form, and ventral branches are stunted; however, directed migrations of the dorsal and visceral branches are largely unaffected. The dorsal trunk also fails to form when FGF or Wingless/WNT signaling is lost, and we show that ribbon functions downstream of, or parallel to, these pathways to promote anterior-posterior migration. Directed cell migration of the salivary gland and dorsal epidermis are also affected in ribbon mutants, suggesting that conserved mechanisms may be employed to orient cell migrations in multiple tissues during development.


2003 ◽  
Vol 256 (2) ◽  
pp. 276-289 ◽  
Author(s):  
Xiaojun Zhao ◽  
Hitoshi Sawa ◽  
Michael A Herman

2004 ◽  
Vol 7 (6) ◽  
pp. 831-841 ◽  
Author(s):  
Timothy Walston ◽  
Christina Tuskey ◽  
Lois Edgar ◽  
Nancy Hawkins ◽  
Gregory Ellis ◽  
...  

Genetics ◽  
2003 ◽  
Vol 164 (4) ◽  
pp. 1355-1367 ◽  
Author(s):  
QueeLim Ch’ng ◽  
Lisa Williams ◽  
Yung S Lie ◽  
Mary Sym ◽  
Jennifer Whangbo ◽  
...  

AbstractIn C. elegans, cells of the QL and QR neuroblast lineages migrate with left-right asymmetry; QL and its descendants migrate posteriorly whereas QR and its descendants migrate anteriorly. One key step in generating this asymmetry is the expression of the Hox gene mab-5 in the QL descendants but not in the QR descendants. This asymmetry appears to be coupled to the asymmetric polarizations and movements of QL and QR as they migrate and relies on an asymmetric response to an EGL-20/Wnt signal. To identify genes involved in these complex layers of regulation and to isolate targets of mab-5 that direct posterior migrations, we screened visually for mutants with cell migration defects in the QL and QR lineages. Here, we describe a set of new mutants (qid-5, qid-6, qid-7, and qid-8) that primarily disrupt the migrations of the QL descendants. Most of these mutants were defective in mab-5 expression in the QL lineage and might identify genes that interact directly or indirectly with the EGL-20/Wnt signaling pathway.


2001 ◽  
Vol 1 (4) ◽  
pp. 491-502 ◽  
Author(s):  
Yi-Chun Wu ◽  
Miao-Chih Tsai ◽  
Li-Chun Cheng ◽  
Chung-Jung Chou ◽  
Nei-Yin Weng

2020 ◽  
Vol 21 (15) ◽  
pp. 5495
Author(s):  
Lai-Sheung Chan ◽  
Hong-Lok Lung ◽  
Roger Kai-Cheong Ngan ◽  
Anne Wing-Mui Lee ◽  
Sai Wah Tsao ◽  
...  

The Wnt signaling pathway is one of the major signaling pathways used by cancer stem cells (CSC). Ecotropic Viral Integration Site 1 (EVI1) has recently been shown to regulate oncogenic development of tumor cells by interacting with multiple signaling pathways, including the Wnt signaling. In the present study, we found that the Wnt modulator ICG-001 could inhibit the expression of EVI1 in nasopharyngeal carcinoma (NPC) cells. Results from loss-of-function and gain-of-function studies revealed that EVI1 expression positively regulated both NPC cell migration and growth of CSC-enriched tumor spheres. Subsequent studies indicated ICG-001 inhibited EVI1 expression via upregulated expression of miR-96. Results from EVI1 3′UTR luciferase reporter assay confirmed that EVI1 is a direct target of miR-96. Further mechanistic studies revealed that ICG-001, overexpression of miR-96, or knockdown of EVI1 expression could restore the expression of miR-449a. The suppressive effect of miR-449a on the cell migration and tumor sphere formation was confirmed in NPC cells. Taken together, the miR-96/EVI1/miR-449a axis is a novel pathway involved in ICG-001-mediated inhibition of NPC cell migration and growth of the tumor spheres.


1999 ◽  
Vol 4 (5) ◽  
pp. 851-858 ◽  
Author(s):  
Jennifer Whangbo ◽  
Cynthia Kenyon

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