Egfr signaling regulates ommatidial rotation and cell motility in the Drosophila eye via MAPK/Pnt signaling and the Ras effector Canoe/AF6

Development ◽  
2003 ◽  
Vol 130 (23) ◽  
pp. 5861-5861
Keyword(s):  
Cell Motility ◽  
Egfr Signaling ◽  
Drosophila Eye ◽  
Ommatidial Rotation

scholarly journals Notch signaling coordinates ommatidial rotation in the Drosophila eye via transcriptional regulation of the EGF-Receptor ligand Argos

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yildiz Koca ◽  
Benjamin E. Housden ◽  
William J. Gault ◽  
Sarah J. Bray ◽  
Marek Mlodzik
Keyword(s):  
Notch Signaling ◽  
Cell Fate ◽  
Planar Cell Polarity ◽  
Egf Receptor ◽  
Control Cell ◽  
Loss Of Function ◽  
Egfr Signaling ◽  
Specific Expression ◽  
Egfr Signaling Pathway ◽  
Ommatidial Rotation

AbstractIn all metazoans, a small number of evolutionarily conserved signaling pathways are reiteratively used during development to orchestrate critical patterning and morphogenetic processes. Among these, Notch (N) signaling is essential for most aspects of tissue patterning where it mediates the communication between adjacent cells to control cell fate specification. In Drosophila, Notch signaling is required for several features of eye development, including the R3/R4 cell fate choice and R7 specification. Here we show that hypomorphic alleles of Notch, belonging to the Nfacet class, reveal a novel phenotype: while photoreceptor specification in the mutant ommatidia is largely normal, defects are observed in ommatidial rotation (OR), a planar cell polarity (PCP)-mediated cell motility process. We demonstrate that during OR Notch signaling is specifically required in the R4 photoreceptor to upregulate the transcription of argos (aos), an inhibitory ligand to the epidermal growth factor receptor (EGFR), to fine-tune the activity of EGFR signaling. Consistently, the loss-of-function defects of Nfacet alleles and EGFR-signaling pathway mutants are largely indistinguishable. A Notch-regulated aos enhancer confers R4 specific expression arguing that aos is directly regulated by Notch signaling in this context via Su(H)-Mam-dependent transcription.

scholarly journals Echinoid regulates Flamingo endocytosis to control ommatidial rotation in the Drosophila eye

Development ◽  
2010 ◽  
Vol 137 (5) ◽  
pp. 745-754 ◽  
Author(s):  
Y.-H. Ho ◽  
M.-T. Lien ◽  
C.-M. Lin ◽  
S.-Y. Wei ◽  
L.-H. Chang ◽  
...  
Keyword(s):  
Drosophila Eye ◽  
Ommatidial Rotation

scholarly journals Carpet Cells Regulate Glial Cell Motility in the Developing Drosophila Eye

2008 ◽  
Vol 28 (11) ◽  
pp. 2686-2687
Author(s):  
P. Cafferty
Keyword(s):  
Cell Motility ◽  
Glial Cell ◽  
Drosophila Eye

EGFR-mediated epidermal stem cell motility drives skin regeneration through COL17A1 proteolysis

2021 ◽  
Vol 220 (11) ◽  
Author(s):  
Daisuke Nanba ◽  
Fujio Toki ◽  
Kyosuke Asakawa ◽  
Hiroyuki Matsumura ◽  
Ken Shiraishi ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Motility ◽  
Mouse Skin ◽  
Skin Regeneration ◽  
Collective Cell Migration ◽  
Egfr Signaling ◽  
Skin Wound Healing ◽  
Functional Link ◽  
Human Keratinocyte ◽  
Epidermal Regeneration

Skin regenerative capacity declines with age, but the underlying mechanisms are largely unknown. Here we demonstrate a functional link between epidermal growth factor receptor (EGFR) signaling and type XVII collagen (COL17A1) proteolysis on age-associated alteration of keratinocyte stem cell dynamics in skin regeneration. Live-imaging and computer simulation experiments predicted that human keratinocyte stem cell motility is coupled with self-renewal and epidermal regeneration. Receptor tyrosine kinase array identified the age-associated decline of EGFR signaling in mouse skin wound healing. Culture experiments proved that EGFR activation drives human keratinocyte stem cell motility with increase of COL17A1 by inhibiting its proteolysis through the secretion of tissue inhibitor of metalloproteinases 1 (TIMP1). Intriguingly, COL17A1 directly regulated keratinocyte stem cell motility and collective cell migration by coordinating actin and keratin filament networks. We conclude that EGFR-COL17A1 axis–mediated keratinocyte stem cell motility drives epidermal regeneration, which provides a novel therapeutic approach for age-associated impaired skin regeneration.

scholarly journals Cooperative activities of Drosophila DE-Cadherin and DN-Cadherin regulate the cell motility process of ommatidial rotation

Development ◽  
2006 ◽  
Vol 133 (17) ◽  
pp. 3283-3293 ◽  
Author(s):  
I. Mirkovic
Keyword(s):  
Cell Motility ◽  
Ommatidial Rotation

scholarly journals Mtlinteracts with members of Egfr signaling and cell adhesion genes in the Drosophila eye

Fly ◽  
2011 ◽  
Vol 5 (2) ◽  
pp. 88-101 ◽  
Author(s):  
Verónica Muñoz-Soriano ◽  
Yaiza Belacortu ◽  
Fabrice C. Durupt ◽  
Silvia Muñoz-Descalzo ◽  
Nuria Paricio
Keyword(s):  
Cell Adhesion ◽  
Egfr Signaling ◽  
Drosophila Eye

scholarly journals Echinoid is essential for regulation of Egfr signaling and R8 formation during Drosophila eye development

Development ◽  
2003 ◽  
Vol 130 (16) ◽  
pp. 3725-3733 ◽  
Author(s):  
S. A. Spencer
Keyword(s):  
Eye Development ◽  
Egfr Signaling ◽  
Drosophila Eye

scholarly journals Split ends antagonizes the Notch and potentiates the EGFR signaling pathways during Drosophila eye development

2007 ◽  
Vol 124 (9-10) ◽  
pp. 792-806 ◽  
Author(s):  
David B. Doroquez ◽  
Terry L. Orr-Weaver ◽  
Ilaria Rebay
Keyword(s):  
Signaling Pathways ◽  
Eye Development ◽  
Egfr Signaling ◽  
Drosophila Eye ◽  
Split Ends

scholarly journals The Novel Plant Homeodomain Protein Rhinoceros Antagonizes Ras Signaling in the Drosophila Eye

Genetics ◽  
2003 ◽  
Vol 165 (4) ◽  
pp. 1993-2006
Author(s):  
Matthew G Voas ◽  
Ilaria Rebay
Keyword(s):  
Mapk Pathway ◽  
Growth Factor Receptor ◽  
Pigment Cells ◽  
Ras Signaling ◽  
Homeodomain Protein ◽  
Egfr Signaling ◽  
Cell Fates ◽  
Regulatory Strategies ◽  
Drosophila Eye ◽  
Fly Eye

Abstract The sequential specification of cell fates in the Drosophila eye requires repeated activation of the epidermal growth factor receptor (EGFR)/Ras/MAP kinase (MAPK) pathway. Equally important are the multiple layers of inhibitory regulation that prevent excessive or inappropriate signaling. Here we describe the molecular and genetic analysis of a previously uncharacterized gene, rhinoceros (rno), that we propose functions to restrict EGFR signaling in the eye. Loss of rno results in the overproduction of photoreceptors, cone cells, and pigment cells and a corresponding reduction in programmed cell death, all phenotypes characteristic of hyperactivated EGFR signaling. Genetic interactions between rno and multiple EGFR pathway components support this hypothesis. rno encodes a novel but evolutionarily conserved nuclear protein with a PHD zinc-finger domain, a motif commonly found in chromatin-remodeling factors. Future analyses of rno will help to elucidate the regulatory strategies that modulate EGFR signaling in the fly eye.

Sign in / Sign up

Export Citation Format

Share Document