AP-1 clathrin adaptor and CG8538/Aftiphilin are involved in Notch signaling during eye development in Drosophila melanogaster

Development ◽  
2012 ◽  
Vol 139 (8) ◽  
pp. e808-e808
Author(s):  
S. Kametaka ◽  
A. Kametaka ◽  
S. Yonekura ◽  
M. Haruta ◽  
S. Takenoshita ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Notch Signaling ◽  
Eye Development ◽  
Clathrin Adaptor

scholarly journals AP-1 clathrin adaptor and CG8538/Aftiphilin are involved in Notch signaling during eye development in Drosophila melanogaster

2012 ◽  
Vol 125 (3) ◽  
pp. 634-648 ◽  
Author(s):  
S. Kametaka ◽  
A. Kametaka ◽  
S. Yonekura ◽  
M. Haruta ◽  
S. Takenoshita ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Notch Signaling ◽  
Eye Development ◽  
Clathrin Adaptor

scholarly journals The physiological control of gene action in the eyeless and eyegone mutants of Drosophila melanogaster

1971 ◽  
Vol 17 (3) ◽  
pp. 195-208 ◽  
Author(s):  
David M. Hunt
Keyword(s):  
Drosophila Melanogaster ◽  
Dietary Supplements ◽  
Pyridoxal Phosphate ◽  
Eye Development ◽  
Metabolic Inhibitors ◽  
Physiological Control ◽  
Eye Size ◽  
Additional Support ◽  
Dietary Treatments ◽  
Mutant Genes

SUMMARYThe effect of dietary supplements of individual l-amino acids on the expression of the eyegone and eyelessK mutants of Drosophila melanogaster are compared. In both mutants, eye size is reduced by excess levels of tryptophan, phenylalanine and methionine, and in each case the effects are independent of metabolic competition for pyridoxal phosphate. A dietary interaction involving methionine and UNA can be demonstrated in the eyK strain, but the mechanism of action of this amino acid is obscure. Tryptophan metabolism is examined in detail. Although both tryptamine and serotonin have significant effects, the action of tryptophan on eye development is largely independent of its metabolic products. Conversely, the effect of dietary supplements of certain catecholamines is consistent with the action of phenylalanine. The action of certain metabolic inhibitors provides additional support for the suggestion that the catecholamines have an important effect on morphogenesis in the eye imaginai disks. Eye development is also affected by increasing concentrations of γ-amino-butyric acid, and this, taken together with the effect of the catecholamines and indolalkylamines, suggests that physiological control of the action of the mutant genes on eye development involves a group of compounds characteristically associated with nervous tissue. Eye development in the eyK strain may be influenced by the availability of acetyl CoA, which would be expected to affect acetylcholine biosynthesis. Possible mechanisms of action of the effective dietary treatments are discussed, together with a tentative hypothesis regarding the mode of action of the mutant genes on eye development.

scholarly journals Role of Notch signaling in establishing the hemilineages of secondary neurons in Drosophila melanogaster

Development ◽  
2009 ◽  
Vol 137 (1) ◽  
pp. 53-61 ◽  
Author(s):  
J. W. Truman ◽  
W. Moats ◽  
J. Altman ◽  
E. C. Marin ◽  
D. W. Williams
Keyword(s):  
Drosophila Melanogaster ◽  
Notch Signaling

scholarly journals Ero1L, a thiol oxidase, is required for Notch signaling through cysteine bridge formation of the Lin12-Notch repeats in Drosophila melanogaster

2008 ◽  
Vol 182 (6) ◽  
pp. 1113-1125 ◽  
Author(s):  
An-Chi Tien ◽  
Akhila Rajan ◽  
Karen L. Schulze ◽  
Hyung Don Ryoo ◽  
Melih Acar ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Notch Signaling ◽  
Cell Fate ◽  
Disulfide Bonds ◽  
Cell Communication ◽  
Notch Receptor ◽  
Cell Fate Decisions ◽  
Unfolded Protein ◽  
Thiol Oxidase ◽  
The Unfolded Protein Response

Notch-mediated cell–cell communication regulates numerous developmental processes and cell fate decisions. Through a mosaic genetic screen in Drosophila melanogaster, we identified a role in Notch signaling for a conserved thiol oxidase, endoplasmic reticulum (ER) oxidoreductin 1–like (Ero1L). Although Ero1L is reported to play a widespread role in protein folding in yeast, in flies Ero1L mutant clones show specific defects in lateral inhibition and inductive signaling, two characteristic processes regulated by Notch signaling. Ero1L mutant cells accumulate high levels of Notch protein in the ER and induce the unfolded protein response, suggesting that Notch is misfolded and fails to be exported from the ER. Biochemical assays demonstrate that Ero1L is required for formation of disulfide bonds of three Lin12-Notch repeats (LNRs) present in the extracellular domain of Notch. These LNRs are unique to the Notch family of proteins. Therefore, we have uncovered an unexpected requirement for Ero1L in the maturation of the Notch receptor.

scholarly journals Gene-environment interactions of the eye-gone mutant in Drosophila melanogaster and a comparison with eyeless

1969 ◽  
Vol 13 (3) ◽  
pp. 313-320 ◽  
Author(s):  
David M. Hunt
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Background ◽  
Eye Development ◽  
Deficient Diet ◽  
Developmental Relationship ◽  
Gene Environment ◽  
Mutant Genes

A comparison of the gene-environment interactions of the eyg mutant in two different genetic backgrounds clearly demonstrates that the properties of the genetic background play a major role in the control of the gene-environment interactions of this mutant. Similarly, modifier background is important in the determination of the sensitive stages in eye development to a cholesterol-deficient diet.The phenotypic identity of the eyeless and eye-gone mutants suggests a close underlying metabolic and developmental relationship. Possible inter-relations of these two mutant genes are discussed in the light of their gene-environment interactions in a standardized genotype.

The dominant Drop eye mutations of Drosophila melanogaster define two loci implicated in normal eye development

1994 ◽  
Vol 244 (4) ◽  
pp. 426-434 ◽  
Author(s):  
Rick Tearle ◽  
Andrew Tomlinson ◽  
Robert Saint
Keyword(s):  
Drosophila Melanogaster ◽  
Eye Development

scholarly journals Delta-1 Activation of Notch-1 Signaling Results inHES-1 Transactivation

1998 ◽  
Vol 18 (12) ◽  
pp. 7423-7431 ◽  
Author(s):  
Sophie Jarriault ◽  
Odile Le Bail ◽  
Estelle Hirsinger ◽  
Olivier Pourquié ◽  
Frédérique Logeat ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Drosophila Melanogaster ◽  
Notch Signaling ◽  
Cell Fate ◽  
Notch Signaling Pathway ◽  
Notch Receptor ◽  
Cell Fate Determination ◽  
Notch 1 ◽  
Promoter Construct ◽  
Enhancer Of Split

ABSTRACT The Notch receptor is involved in many cell fate determination events in vertebrates and invertebrates. It has been shown inDrosophila melanogaster that Delta-dependent Notch signaling activates the transcription factor Suppressor of Hairless, leading to an increased expression of the Enhancer of Splitgenes. Genetic evidence has also implicated the kuzbaniangene, which encodes a disintegrin metalloprotease, in the Notch signaling pathway. By using a two-cell coculture assay, we show here that vertebrate Dl-1 activates the Notch-1 cascade. Consistent with previous data obtained with active forms of Notch-1 aHES-1-derived promoter construct is transactivated in cells expressing Notch-1 in response to Dl-1 stimulation. Impairing the proteolytic maturation of the full-length receptor leads to a decrease in HES-1 transactivation, further supporting the hypothesis that only mature processed Notch is expressed at the cell surface and activated by its ligand. Furthermore, we observed that Dl-1-inducedHES-1 transactivation was dependent both on Kuzbanian and RBP-J activities, consistent with the involvement of these two proteins in Notch signaling in Drosophila. We also observed that exposure of Notch-1-expressing cells to Dl-1 results in an increased level of endogenous HES-1 mRNA. Finally, coculture of Dl-1-expressing cells with myogenic C2 cells suppresses differentiation of C2 cells into myotubes, as previously demonstrated for Jagged-1 and Jagged-2, and also leads to an increased level of endogenousHES-1 mRNA. Thus, Dl-1 behaves as a functional ligand for Notch-1 and has the same ability to suppress cell differentiation as the Jagged proteins do.

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