Maheshvara, a Conserved RNA Helicase, Regulates Notch Signaling in Drosophila melanogaster

2020 ◽  
pp. 69-79
Author(s):  
Bhawana Maurya ◽  
Satya Surabhi ◽  
Ashim Mukherjee ◽  
Mousumi Mutsuddi
Keyword(s):  
Drosophila Melanogaster ◽  
Notch Signaling ◽  
Rna Helicase

scholarly journals Regulation of Notch Signaling by an Evolutionary Conserved DEAD Box RNA Helicase, Maheshvara in Drosophila melanogaster

Genetics ◽  
2015 ◽  
Vol 201 (3) ◽  
pp. 1071-1085 ◽  
Author(s):  
Satya Surabhi ◽  
Bipin K. Tripathi ◽  
Bhawana Maurya ◽  
Pradeep K. Bhaskar ◽  
Ashim Mukherjee ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Notch Signaling ◽  
Rna Helicase ◽  
Dead Box

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.

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 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.

scholarly journals RNA helicase Ddx5 and the noncoding RNA SRA act as coactivators in the Notch signaling pathway

2013 ◽  
Vol 1833 (5) ◽  
pp. 1180-1189 ◽  
Author(s):  
Claudia Jung ◽  
Gerhard Mittler ◽  
Franz Oswald ◽  
Tilman Borggrefe
Keyword(s):  
Notch Signaling ◽  
Signaling Pathway ◽  
Noncoding Rna ◽  
Rna Helicase ◽  
Notch Signaling Pathway

scholarly journals Regulation of Notch Signaling by a Novel Mechanism Involving Suppressor of Hairless Stability and Carboxyl Terminus-Truncated Notch

2003 ◽  
Vol 23 (16) ◽  
pp. 5581-5593 ◽  
Author(s):  
Cedric S. Wesley ◽  
Lee-Peng Mok
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Drosophila Melanogaster ◽  
Notch Signaling ◽  
Full Length ◽  
Carboxyl Terminus ◽  
Animal Development ◽  
Suppressor Of Hairless ◽  
The Central Nervous System ◽  
Different Tissues

ABSTRACT Different amounts of Suppressor of Hairless (SuH)-dependent Notch (N) signaling is often used during animal development to produce two different tissues from a population of equipotent cells. During Drosophila melanogaster embryogenesis, cells with high amounts of this signaling differentiate the larval epidermis whereas cells with low amounts, or none, differentiate the central nervous system (CNS). The mechanism by which SuH-dependent N signaling is increased or decreased in these different cells is obscure. The developing epidermis is known to get enriched for the full-length N (NFull) and the developing CNS for the carboxyl terminus-truncated N (NΔCterm). Results described here indicate that this differential accumulation of N receptors is part of a mechanism that would promote SuH-dependent N signaling in the developing epidermis but suppress it in the developing CNS. This mechanism involves SuH-dependent stability of NFull, NFull-dependent accumulation of SuH, stage specific stability of SuH, and NΔCterm-dependent loss of SuH and NFull.

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