scholarly journals CoREST acts as a positive regulator of Notch signaling in the follicle cells of Drosophila melanogaster

2012 ◽  
Vol 125 (2) ◽  
pp. 399-410 ◽  
Author(s):  
E. Domanitskaya ◽  
T. Schupbach
2011 ◽  
Vol 356 (1) ◽  
pp. 128-129
Author(s):  
Elena Domanitskaya ◽  
Trudi Schupbach

Development ◽  
2012 ◽  
Vol 139 (6) ◽  
pp. e608-e608
Author(s):  
E. Domanitskaya ◽  
T. Schupbach

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

2008 ◽  
Vol 182 (6) ◽  
pp. 1113-1125 ◽  
Author(s):  
An-Chi Tien ◽  
Akhila Rajan ◽  
Karen L. Schulze ◽  
Hyung Don Ryoo ◽  
Melih Acar ◽  
...  

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.


2008 ◽  
Vol 319 (2) ◽  
pp. 527-528
Author(s):  
Yan Yan ◽  
Natalie Denef ◽  
Trudi Schupbach

Development ◽  
2012 ◽  
Vol 139 (8) ◽  
pp. e808-e808
Author(s):  
S. Kametaka ◽  
A. Kametaka ◽  
S. Yonekura ◽  
M. Haruta ◽  
S. Takenoshita ◽  
...  

1998 ◽  
Vol 18 (12) ◽  
pp. 7423-7431 ◽  
Author(s):  
Sophie Jarriault ◽  
Odile Le Bail ◽  
Estelle Hirsinger ◽  
Olivier Pourquié ◽  
Frédérique Logeat ◽  
...  

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.


Sign in / Sign up

Export Citation Format

Share Document