Cell Cycle Part 3: Apoptosis
Cell Biology Oct.3/14
Cell Cycle part 3: Apoptosis
2 Main ways cells will die: apoptosis is regulated, nacrosis is an “explosion”
Apoptosis
Part of controling number of cells. Importance in balance.“Programmed cell death” – important because if the cell isn’t intact you don’t want cell to divide and keep mutations going, to avoid inflammatory response (caused by cells that exploded/necrosis).. ect.
Necrosis is triggered by something unplanned, leading to decrease ATP, pumps, atpase activity, membrane becomes permeable = lysis, Caused by trauma or cytotoxicity. Now all of these organelles and enzymes ect are in the neighboring cells which cause problems to healthy cells.
By apoptosis you can get rid of cell without impact on neighbouring …show more content…
Orderly disposal of dead cell.
Structural changes during apoptosis
First there is condensation of chromatin in nucleus, and cytoplasm will shrink. Nucleus becomes fragmented. DNA will be cut into small portions = DNA laddering. - - Important hallmark of apoptosis because as DNA becomes fragmented the ends of fragments can be used to detect and confirm that it is actually apoptosis.
Portions of the cell will form vesicles that contain part of dna and organells wrapped in membrane = blebbing. These blebs are called apoptotic bodies. Neighbouring cells will be able to absorb blebs and get rid of them = phagocytosis. No enzymes/proteins ect are outside because everything is in the bleb.
PhagocytisisHow do you target blebs so that neighbouring cells know to swallow them?
Bilipid layer membrane has neg polar heads(phosphatidylserine) inside but when bleb is formed they are flipped pointing to the outside layer. This triggers the reaction. Detect the vesicles as having an anomaly in the membrane. Macrophage (white blood cell) and other cells will start …show more content…
Amplification – one signal = many caspases activate and work towards cell death.
2 major pathways
Extrinsic : procaspace activation triggered by outside factor that interacts with receptors in the cell membrane called cell death receptors.
Intrinsic : something inside the cell triggers procaspase activation and this may or may not involve SF. You’d think but SF are outside of cell? Well in the absence of SF it’s this absence that triggers apoptosis therefore intracellular response. Also possible by intracellular damage.Extrinsic pathway
Signal is called Fas(protein that is expressed on surface of cells) ligand. Mostly used in immunology. Eg. Killer lymphocytes will use these pathways to direct cells to be apoptosed.
They express Fas ligand that will bind to death receptor – the fas death receptor.
Fas bound to receptor triggers a conformational change within cell.
Receptor can now interact with subunits of protein called FAD (adaptor protein, fas associated death domain).
FAD will recruit procaspace – the initiator procaspace (inactive). Forms death inducing complex called DISC which leads to cleavage of initiator caspase which makes it active. The active caspases will activate more via proteolytic
Cell Cycle part 3: Apoptosis
2 Main ways cells will die: apoptosis is regulated, nacrosis is an “explosion”
Apoptosis
Part of controling number of cells. Importance in balance.“Programmed cell death” – important because if the cell isn’t intact you don’t want cell to divide and keep mutations going, to avoid inflammatory response (caused by cells that exploded/necrosis).. ect.
Necrosis is triggered by something unplanned, leading to decrease ATP, pumps, atpase activity, membrane becomes permeable = lysis, Caused by trauma or cytotoxicity. Now all of these organelles and enzymes ect are in the neighboring cells which cause problems to healthy cells.
By apoptosis you can get rid of cell without impact on neighbouring …show more content…
Orderly disposal of dead cell.
Structural changes during apoptosis
First there is condensation of chromatin in nucleus, and cytoplasm will shrink. Nucleus becomes fragmented. DNA will be cut into small portions = DNA laddering. - - Important hallmark of apoptosis because as DNA becomes fragmented the ends of fragments can be used to detect and confirm that it is actually apoptosis.
Portions of the cell will form vesicles that contain part of dna and organells wrapped in membrane = blebbing. These blebs are called apoptotic bodies. Neighbouring cells will be able to absorb blebs and get rid of them = phagocytosis. No enzymes/proteins ect are outside because everything is in the bleb.
PhagocytisisHow do you target blebs so that neighbouring cells know to swallow them?
Bilipid layer membrane has neg polar heads(phosphatidylserine) inside but when bleb is formed they are flipped pointing to the outside layer. This triggers the reaction. Detect the vesicles as having an anomaly in the membrane. Macrophage (white blood cell) and other cells will start …show more content…
Amplification – one signal = many caspases activate and work towards cell death.
2 major pathways
Extrinsic : procaspace activation triggered by outside factor that interacts with receptors in the cell membrane called cell death receptors.
Intrinsic : something inside the cell triggers procaspase activation and this may or may not involve SF. You’d think but SF are outside of cell? Well in the absence of SF it’s this absence that triggers apoptosis therefore intracellular response. Also possible by intracellular damage.Extrinsic pathway
Signal is called Fas(protein that is expressed on surface of cells) ligand. Mostly used in immunology. Eg. Killer lymphocytes will use these pathways to direct cells to be apoptosed.
They express Fas ligand that will bind to death receptor – the fas death receptor.
Fas bound to receptor triggers a conformational change within cell.
Receptor can now interact with subunits of protein called FAD (adaptor protein, fas associated death domain).
FAD will recruit procaspace – the initiator procaspace (inactive). Forms death inducing complex called DISC which leads to cleavage of initiator caspase which makes it active. The active caspases will activate more via proteolytic