The slide describes apoptosis via two pathways: the extrinsic pathway, triggered by extracellular ligands binding death receptors (e.g., Fas, TNFR1), recruiting FADD to activate caspase-8 through DISC formation, and mitochondria-independent. The intrinsic pathway is initiated by intracellular stress (e.g., DNA damage), with Bcl-2 family proteins regulating mitochondrial cytochrome c release to form an apoptosome and activate caspase-9, converging on effector caspases.
Mechanisms of Apoptosis
| Extrinsic Pathway (Death Receptors) | Intrinsic Pathway (Mitochondrial) |
|---|
| Triggered by extracellular ligands binding death receptors (e.g., Fas, TNFR1). Recruits FADD and activates initiator caspase-8 via DISC formation. Amplifies signal through Bid cleavage or direct effector caspase activation. Mitochondria-independent. | Initiated by intracellular stress (DNA damage, hypoxia). Bcl-2 family regulates MOMP, releasing cytochrome c. Forms apoptosome with Apaf-1, activating caspase-9. Converges on effector caspases for demolition phase. |
Source: Adapted from Molecular Biology of the Cell, Alberts et al.
Speaker Notes
Discuss extrinsic vs intrinsic pathways; note convergence on caspases. Image depicts microscopy of apoptotic cells showing membrane blebbing.