EGF-Receptor Signaling in Caenorhabditis elegans Vulval Development

2003 ◽  
pp. 805-808
Author(s):  
Nadeem Moghal ◽  
Paul W. Sternberg
2006 ◽  
Vol 25 (11) ◽  
pp. 2347-2357 ◽  
Author(s):  
Attila Stetak ◽  
Erika Fröhli Hoier ◽  
Assunta Croce ◽  
Giuseppe Cassata ◽  
Pier Paolo Di Fiore ◽  
...  

Development ◽  
2022 ◽  
Vol 149 (1) ◽  
Author(s):  
Silvan Spiri ◽  
Simon Berger ◽  
Louisa Mereu ◽  
Andrew DeMello ◽  
Alex Hajnal

ABSTRACT During Caenorhabditis elegans vulval development, the uterine anchor cell (AC) first secretes an epidermal growth factor (EGF) to specify the vulval cell fates and then invades the underlying vulval epithelium. By doing so, the AC establishes direct contact with the invaginating primary vulF cells and attaches the developing uterus to the vulva. The signals involved and the exact sequence of events joining these two organs are not fully understood. Using a conditional let-23 EGF receptor (EGFR) allele along with novel microfluidic short- and long-term imaging methods, we discovered a specific function of the EGFR in the AC during vulval lumen morphogenesis. Tissue-specific inactivation of let-23 in the AC resulted in imprecise alignment of the AC with the primary vulval cells, delayed AC invasion and disorganized adherens junctions at the contact site forming between the AC and the dorsal vulF toroid. We propose that EGFR signaling, activated by a reciprocal EGF cue from the primary vulval cells, positions the AC at the vulval midline, guides it during invasion and assembles a cytoskeletal scaffold organizing the adherens junctions that connect the developing uterus to the dorsal vulF toroid. Thus, EGFR signaling in the AC ensures the precise alignment of the two developing organs.


2001 ◽  
Author(s):  
Brian Ceresa ◽  
Sandra L. Schmid

2005 ◽  
Vol 102 (14) ◽  
pp. 4972-4977 ◽  
Author(s):  
T. Inoue ◽  
M. Wang ◽  
T. O. Ririe ◽  
J. S. Fernandes ◽  
P. W. Sternberg

Diabetes ◽  
2006 ◽  
Vol 55 (12) ◽  
pp. 3299-3308 ◽  
Author(s):  
P. J. Miettinen ◽  
J. Ustinov ◽  
P. Ormio ◽  
R. Gao ◽  
J. Palgi ◽  
...  

2004 ◽  
Vol 24 (2) ◽  
pp. 796-808 ◽  
Author(s):  
Lindsay K. MacDougall ◽  
Mary Elizabeth Gagou ◽  
Sally J. Leevers ◽  
Ernst Hafen ◽  
Michael D. Waterfield

ABSTRACT Phosphoinositide 3-kinases (PI3Ks) can be divided into three distinct classes (I, II, and III) on the basis of their domain structures and the lipid signals that they generate. Functions have been assigned to the class I and class III enzymes but have not been established for the class II PI3Ks. We have obtained the first evidence for a biological function for a class II PI3K by expressing this enzyme during Drosophila melanogaster development and by using deficiencies that remove the endogenous gene. Wild-type and catalytically inactive PI3K_68D transgenes have opposite effects on the number of sensory bristles and on wing venation phenotypes induced by modified epidermal growth factor (EGF) receptor signaling. These results indicate that the endogenous PI3K_68D may act antagonistically to the EGF receptor-stimulated Ras-mitogen-activated protein kinase pathway and downstream of, or parallel to, the Notch receptor. A class II polyproline motif in PI3K_68D can bind the Drk adaptor protein in vitro, primarily via the N-terminal SH3 domain of Drk. Drk may thus be important for the localization of PI3K_68D, allowing it to modify signaling pathways downstream of cell surface receptors. The phenotypes obtained are markedly distinct from those generated by expression of the Drosophila class I PI3K, which affects growth but not pattern formation.


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