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CD95 capping is ROCK-dependent and dispensable for apoptosis
Thomas S Söderström1, Sofia D Nyberg, John E Eriksson
1Department of Biology, Abo Akademi University, FI-20520, Turku, Finland.
Journal of Cell Science
|April 28, 2005
Summary
CD95 receptor capping in lymphocytes does not induce apoptosis. This process involves actin cytoskeleton and lipid raft reorganization, regulated by Rho kinase (ROCK) signaling, suggesting roles in non-apoptotic functions.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- CD95 receptor engagement triggers rapid cellular 'capping'.
- CD95 capping is proposed to initiate apoptotic signaling.
- The precise biological roles of CD95 capping remain unclear.
Purpose of the Study:
- To investigate the role of CD95 capping in lymphocyte apoptosis induction.
- To elucidate the signaling pathways regulating CD95 capping and cellular polarization.
Main Methods:
- Investigated CD95 capping in type I and type II cells.
- Examined the effects of inhibiting actin polymerization and caspase-8.
- Assessed Rho kinase (ROCK) and RhoA signaling pathways.
Main Results:
- CD95 capping is uncoupled from apoptosis; they can occur independently.
- CD95 capping correlates with actin cytoskeleton reorganization and lipid raft aggregation.
- Cellular polarization during CD95 capping is ROCK-dependent, with distinct activation mechanisms in type I and type II cells.
- ROCK activation is caspase-dependent in type I cells, while CD95 activates RhoA in type II cells.
Conclusions:
- CD95 capping and cellular polarization are ROCK-regulated processes.
- These events do not correlate with apoptosis induction.
- CD95 capping is likely involved in non-apoptotic functions of CD95.