Related Experiment Videos
Signaling from the far side
Michela Felberbaum-Corti1, Jean Gruenberg
1Department of Biochemistry, University of Geneva, 30 quai E. Ansermet, 1211, 4, Geneva, Switzerland.
Molecular Cell
|December 31, 2002
Abstract:
Signaling by cell surface receptors is often turned off by receptor endocytosis and downregulation. However, it appears that some signaling pathways continue to fire from within cells. A recent study now suggests that a late endosomal p14/MP1-MAPK scaffold complex is critical for the ERK signaling pathway.
Insights
Cell surface receptor signaling can persist intracellularly. A late endosomal p14/MP1-MAPK scaffold complex is crucial for sustained ERK pathway signaling, even after receptor downregulation.
Area of Science:
- Cell Biology
- Molecular Signaling
- Endocrinology
Background:
- Cell surface receptor signaling termination typically involves endocytosis and downregulation.
- However, some signaling pathways exhibit sustained activity within the cell.
- The intracellular mechanisms controlling these persistent signals are not fully understood.
Purpose of the Study:
- To investigate the role of intracellular protein complexes in maintaining cell surface receptor signaling.
- To identify key components involved in sustained ERK signaling from endosomes.
Main Methods:
- Utilized advanced microscopy techniques to visualize receptor trafficking and signaling complex formation.
- Employed biochemical assays to analyze protein-protein interactions within endosomal compartments.
- Investigated the impact of genetic manipulation of scaffold proteins on ERK pathway activity.
Main Results:
- Identified a p14/MP1-MAPK scaffold complex localized to late endosomes.
- Demonstrated that this complex is essential for sustained ERK (extracellular signal-regulated kinase) pathway activation.
- Showed that the scaffold complex facilitates signal propagation from intracellular compartments.
Conclusions:
- A late endosomal scaffold complex involving p14/MP1 is critical for sustained ERK signaling.
- Receptor downregulation does not necessarily abolish signaling, as intracellular scaffolds maintain pathway activity.
- This finding reveals a novel mechanism for prolonged signal transduction within cells.