BIOL 212 Lecture Notes - Lecture 32: Mitochondrion, Fas Ligand, Cytochrome C
18 May 2018
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Lecture Notes 32
2 Ways Kill a Cell
- Apoptosis- programmed cell death
- Necrosis- explode
Apoptosis
- Cell shrinkage
- Plasma membrane integrity is preserved (until later stages)
- Depolarization and permeabilization of mitochondria; release of cytochrome c
- Disassembly of nuclear envelope; condensation and fragmentation of nuclear DNA
- Alterations of cell surface that promote phagocytosis
- Planned and neat
- Induced by EC signals (DISC death-inducing signaling complex) Fas ligand that activate caspases
- Cells can induce apoptosis internally
o Bax and Bak form channels in outer mitochondrial membrane , release cytochrome C, adaptor
protein activated, procaspase-9 molecules leads to caspase cascade
- Engulfed by macrophages
- Apoptotic cell changes its cell surface properties to signal for engulfment
- Undergo many cell surface changes
o Exposure of phosphatidylserine: normally phosphatidylserine (PS) is located in cytosolic half of
lipid bilayer
- Release of cytochrome c → exposure of phosphatidylserine → increased permeability of the plasma
membrane
Necrosis
- Result of acute injury
- Cell swelling and bursting
- Spilling of cell contents
- Causes inflammatory response
- Accidental and messy
Limb Development
- Important role in limb development, apoptosis
- Developing mouse limb
- Tails of amphibian and ascidian tadpoles eliminated by apoptosis
Nervous System
- Extra cells in nervous system eliminated by apoptosis, ensures every target cell contacted by single
neuron, extra neuron eliminated
Tightly Controlled
- Important to development of organism
- Balance of cell survival and cell death necessary for maintenance of tissue architecture
- Such balance maintained by signal that either promote or inhibit apoptosis
- Either two little or too much cell death leads to disease states (autoimmune, neurodegeneration, cancer)
- Important in adult to eliminate damaged cells
C. elegans
- genes involved in cell death were originally identified in the nematode
- pre-determined set cells is destined for apoptosis in C. elegans
- mutations in “death genes” will result in extra cells and overgrowth of organs
- such gens identified in systematic genetic screens of C. elegans
Caspases
- key proteases in apoptosis, activated by proteolysis at specific types
- NH2 and COOh two inactive procaspase molecules, activated by cleavage
- Apoptosis stimulated by caspase cascade
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Document Summary
Plasma membrane integrity is preserved (until later stages) Depolarization and permeabilization of mitochondria; release of cytochrome c. Disassembly of nuclear envelope; condensation and fragmentation of nuclear dna. Alterations of cell surface that promote phagocytosis. Induced by ec signals (disc death-inducing signaling complex) fas ligand that activate caspases. Cells can induce apoptosis internally: bax and bak form channels in outer mitochondrial membrane , release cytochrome c, adaptor protein activated, procaspase-9 molecules leads to caspase cascade. Apoptotic cell changes its cell surface properties to signal for engulfment. Undergo many cell surface changes: exposure of phosphatidylserine: normally phosphatidylserine (ps) is located in cytosolic half of lipid bilayer. Release of cytochrome c exposure of phosphatidylserine increased permeability of the plasma membrane. Tails of amphibian and ascidian tadpoles eliminated by apoptosis. Extra cells in nervous system eliminated by apoptosis, ensures every target cell contacted by single neuron, extra neuron eliminated. Balance of cell survival and cell death necessary for maintenance of tissue architecture.
