Related Experiment Video

Updated: Aug 11, 2026

Live-imaging of the Drosophila Pupal Eye
09:54

Live-imaging of the Drosophila Pupal Eye

Published on: January 12, 2015

EGF receptor/Rolled MAP kinase signalling protects cells against activated Armadillo in the Drosophila eye

M Freeman1, M Bienz

  • 1MRC Laboratory of Molecular Biology, Cambridge, UK.

EMBO Reports
|March 22, 2001
PubMed

Insights

Activated beta-catenin (also known as Armadillo) drives cancer. In Drosophila, EGF receptor signaling specifically prevents activated Armadillo from causing cell death, revealing a crucial negative control mechanism.

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Beta-catenin/Armadillo proteins are key transcriptional co-activators in Wnt signaling during development.
  • Aberrant activation of beta-catenin is implicated in oncogenesis.
  • Understanding the regulation of activated beta-catenin is crucial for cancer research.

Purpose of the Study:

  • To investigate the effects of oncogenic mutations of Drosophila Armadillo.
  • To identify regulatory mechanisms controlling activated Armadillo in vivo.
  • To explore the role of specific signaling pathways in mediating the cellular response to activated Armadillo.

Main Methods:

  • Construction and expression of mutant Drosophila Armadillo forms mimicking human oncogenic mutations.
  • Analysis of cell fate and apoptosis in the Drosophila eye following Armadillo activation.
  • Investigating the role of Epidermal Growth Factor Receptor (EGFR)/MAP kinase signaling in modulating Armadillo's effects.
  • Assessing the interaction between Nemo (a MAP kinase) and activated Armadillo.

Main Results:

  • Constitutively activated Armadillo mutants were generated and expressed in the Drosophila eye.
  • Activated Armadillo induced apoptosis across all cell types, but with a significant latency period.
  • Epidermal Growth Factor Receptor (EGFR)/MAP kinase signaling conferred resistance to activated Armadillo-induced apoptosis.
  • EGFR/MAP kinase signaling cessation led to rapid cell death.
  • Nemo, a homolog of mammalian NLK, did not antagonize activated Armadillo.

Conclusions:

  • Activated Armadillo is subject to specific negative regulation by EGFR/MAP kinase signaling.
  • EGFR/MAP kinase signaling acts as a critical gatekeeper, delaying apoptosis induced by activated Armadillo.
  • The Nemo-like kinase pathway may not generally interact with Armadillo/beta-catenin in this context.

More Related Videos

Spatial and Temporal Analysis of Active ERK in the C. elegans Germline08:40

Spatial and Temporal Analysis of Active ERK in the C. elegans Germline

Published on: November 29, 2016

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans08:12

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans

Published on: October 5, 2020

Related Concept Videos

Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.