Lec 42 Flashcards
Cell necrosis
Injured cell ruptures and damages neighboring cells
Apoptosis
Cells that are no longer needed are dismantled
Preparation for apoptosis
Procaspases are present but inactive in the cell
Bcl2 protects mitochondria
DNases are inactive in nucleus
Phosphatidylserines are hidden in membrane
Step 1 of apoptosis
The trigger
Triggers for apoptosis
Damage to mitochondria
Damage to DNA
Absence of survival signals
Death signal from a T cell (type of WBC)
Survival signalsT
Many neurons are released to a target cell
When one reaches the target, the target releases survival signals indicating that the neurons works
T cells
Sees a virus in a an adjacent cell and sends a death signal
contact dependent signalling
Activation of procaspases
A signal comes along and makes active caspases which cause apoptosis
Procaspases are activated by
Proteolysis
cutting of certain pieces and rearrangement of others
Adaptor protein
brings procaspases together and causes proteolysis to all of them to activate them
Healthy mitochondria
Healthy inner and outer membrane
Cytochrome c is inside the mitochondria
If mitochondria is damage
cytochrome c is released to signal apoptosis
Procaspases are brought together and made into caspases
DNA damage leads to
p53 which leads to creation of PUMA
PUMA inhibits Bcl2
Bcl2 protects the mitochondria so its inhibition causes Cytochrome c to be released which leads to caspases like before
UV can cause
DNA damage
Absence of survival signals leads to
no Bcl2 is made
Cyt c released
same as before
T cells have
Fas ligands which attach to Fas receptor on infected cells
Death signal from a T cell leads to
Fas ligands attaching to Fas receptor
This leads to Procaspases being brought together and the rest is the same
Caspase cascade
Once one caspase is activated they activated all the other 6 types of procaspases
Chain reaction
Caspases also
Cleave target proteins
Cell destruction
Chromosome destruction
Caspases indirectly activate DNase by destroying its inhibitor
Destroying the chromosomes
DNase chops between every histone (about every 200bp)
Experiment apoptosis
Adding DNA repair enzymes and fluorescently labelled DNA nucleotides
Them binding to the apoptosis cells makes them fluoresce
Experiment called TUNEL
Madagascar Laceleaf
Grows in streams with water pushing against it
Plant has holes in the leaf to allow it to stand upright which is done by apoptosis
Nuclear envelope being dismantled
Caspases directly destroy Nuclear Lamins
cells then round up and become apoptotic bodies
Caspases target
Everything (nucleus and everything the cell is connected to)
What happens to the little of pieces of cells (apoptotic bodies)
Phagocytosis by either neighbor cells or macrophages
Non-professional phagocytes
Neighboring cells
Professional phagocytes
Macrophages
Phosphatidylserine
Move to outer side of membrane from the inner
to tell other cells to consume the apoptotic bodies
Scramblase
Scramble Phosphatidylserine
Flipase
Flip Phosphatidylserine
Phosphatidylserine moving to the outside is done by
Neither flipase or scramblase
Instead exocytosis and endocytosis is done poorly and randomly to scramble the Phosphatidylserines and put some of them of the outside
Why chop up DNA
To make apoptosis irreversible
To make apoptotic bodies safe to eat (destroy viruses)
