Dishevelled is a component of the frizzled signaling pathway in Drosophila

Development ◽  
1995 ◽  
Vol 121 (12) ◽  
pp. 4095-4102 ◽  
Author(s):  
R.E. Krasnow ◽  
L.L. Wong ◽  
P.N. Adler
Keyword(s):  
Signal Transduction ◽  
Cell Polarity ◽  
Signal Transduction Pathway ◽  
Receptor Complex ◽  
Transduction Pathway ◽  
General Role ◽  
Tissue Polarity ◽  
Developmental Patterning ◽  
Single Process ◽  
Genetic Hierarchy

The tissue polarity genes in Drosophila are required to coordinate cell polarity within the plane of the epidermis. Evidence to date suggests that these genes may encode components of a novel signal transduction pathway. Three of the genes, frizzled (fz), dishevelled (dsh), and prickle (pk) share a similar tissue polarity phenotype, suggesting that they function together in a single process. dsh is also known to function as a mediator of wingless (wg) signaling in a variety of developmental patterning processes in the fly. In this study, we make use of a fz transgene and a hypomorphic fz allele as genetic tools in an attempt to order these genes in a genetic hierarchy. Our results argue that dsh encodes a dosage sensitive component required for fz function and that it likely acts downstream of fz in the generation of tissue polarity. Our findings suggest that dsh may have a general role in signal transduction, perhaps as a component of a receptor complex.

scholarly journals Van Gogh: A New Drosophila Tissue Polarity Gene

Genetics ◽  
1998 ◽  
Vol 150 (1) ◽  
pp. 199-210 ◽  
Author(s):  
Job Taylor ◽  
Natasha Abramova ◽  
Jeannette Charlton ◽  
Paul N Adler
Keyword(s):  
Signal Transduction ◽  
Signal Transduction Pathway ◽  
Strong Interactions ◽  
Transduction Pathway ◽  
Van Gogh ◽  
Tissue Polarity ◽  
Autonomous Function ◽  
Cuticular Structures ◽  
Adult Drosophila ◽  
Polarity Gene

Abstract Mutations in the Van Gogh gene result in the altered polarity of adult Drosophila cuticular structures. On the wing, Van Gogh mutations cause an altered polarity pattern that is typical of mutations that inactivate the frizzled signaling/signal transduction pathway. The phenotype however, differs from those seen previously, as the number of wing cells forming more than one hair is intermediate between that seen previously for typical frizzled-like or inturned-like mutations. Consistent with Van Gogh being involved in the function of the frizzled signaling/signal transduction pathway, Van Gogh mutations show strong interactions with mutations in frizzled and prickle. Mitotic clones of Van Gogh display domineering cell nonautonomy. In contrast to frizzled clones, Van Gogh clones alter the polarity of cells proximal (and in part anterior and posterior) but not distal to the clone. In further contrast to frizzled clones, Van Gogh clones cause neighboring wild-type hairs to point away from rather than toward the clone. This anti-frizzled type of domineering nonautonomy and the strong genetic interactions seen between frizzled and Van Gogh suggested the possibility that Van Gogh was required for the noncell autonomous function of frizzled. As a test of this possibility we induced frizzled clones in a Van Gogh mutant background and Van Gogh clones in a frizzled mutant background. In both cases the domineering nonautonomy was suppressed consistent with Van Gogh being essential for frizzled signaling.

Cell polarity and locomotion, as well as endocytosis, depend on NSF

Development ◽  
2002 ◽  
Vol 129 (18) ◽  
pp. 4185-4192 ◽  
Author(s):  
Chris R. L. Thompson ◽  
Mark S. Bretscher
Keyword(s):  
Signal Transduction ◽  
Cell Polarity ◽  
Surface Membrane ◽  
Signal Transduction Pathway ◽  
Temperature Sensitive ◽  
Membrane Recycling ◽  
Transduction Pathway ◽  
Tentative Model ◽  
Sensitive Factor ◽  
A Cell

NEM-sensitive factor (NSF) is an essential protein required during membrane transport. We replaced part of the endogenous D. discoideum NSF gene (nsfA) by a PCR-mutagenised library and isolated 11 mutants temperature-sensitive (ts) for growth. Two of these have been studied in detail. As expected, both are ts for FITC-dextran uptake by macropinocytosis, for internalising their surface membrane (monitored with FM1-43) and for phagocytosis. However, after 10-20 minutes at 28°C, they round up and cease to chemotax, move or cap ConA receptors. They fully recover when returned to 22°C. These cells carry out a normal ‘cringe’ reaction in response to cAMP, indicating that the actin cytoskeleton and this signal transduction pathway are still functional at 28°C. The behaviour of these mutants shows that NSF-catalysed processes are required not only for the different endocytic cycles but also for the maintenance of cell polarity. As cell locomotion depends on a cell having a polarity, the mutants stop moving at high temperature. A tentative model is proposed to explain the surprising link between membrane recycling and cell polarity revealed here.

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