suicide and death (hekimi) Flashcards
how were we able to shape our fingers to get rid of the skin between our fingers? what does this show us
shaping done by killing cells. proves that cell death is essential in development
give an example of how cell death is necessary during brain development
-many motor neurons develop connecting the nervous system to the limbs (more than we need), in order to make sure that the limbs get properly innervated
-all those that arent necessary die by apoptosis
what is apoptosis?
cell death
explain
-only motor neurons with target survive (target capable of sustaining them)
-Those that fail to make proper connections undergo apoptosis, ensuring precise motor control.
whats the link between apoptosis at development and autism?
-if usuless neurons fail to undergo apoptosis, can lead to autism
what does the apoptosis network do?
-its there to take into account all internal and external factors to figure out if the cell should die
difference types of apoptosis?
-developmental apoptosis (apoptosis necessary for development)
-homostatic apoptosis: destroying cell thats unhealthy, in order to prevent dying cells from damaging its nerighbours
other than apoptosis, what are 2 other types of cell deaths?
-necrosis: uncrontrolled, unregulated, cell death. Cells explode and release all their contents, triggering inflammation. response to trauma, infections
-autophagy: cell eats itself (digests its own constituents until it dies)
true or false, autophagy is uncontrolled and unplanned
false, its programmed cell death
what is the hypothesis about the hybrid between apoptosis and necrosis?
Necroptosis is a mix of apoptosis and necrosis:
-Like apoptosis, Controlled, genetically regulated.
-Like necrosis, Triggers inflammation (cell bursts).
can be used as a backup to apoptosis when apoptosis signalling pathway is blocked by endogenous or exogenous factors such as viruses or mutations
what are the steps of destruction in self-destruction?
what are the CED genes?
-genes that code for proteins essential in the cell death process
-discovereed in c elegans
-their mutation leads to issues with cell death (the three little bumps in the c elegans wont be present anymore)
what are caspases?
-effector proteins, agents of death in apoptosis
-they are proteases with particular targets
-involved in the cascade leading to apoptosis
true or false, apoptosis in c elegans is identical to apoptosis in vertebrates
false, simpler in c elegans
what triggers apoptosis in c elegans? describe process
-release of CED-4 from mitochondria
-CED-4 released from its binding with CED-9, and will then go form an octamer
-will then go bind to CED-3 (inactive caspase initially)
-CED-4/CED-3 caspase holoenzyme is now an active caspase, which will trigger the cell death process
what disrupts the CED-9/CED-4 in c elegans? what does this do?
EGL-1
-Binds to CED-9, leaving CED-4 free to trigger destruction process
-signals if cell should die
how does EGL-1 act in the development of a male c elegan?
-all c elegans start as hemaphrodites, therefore the HSN is expressed during their development
-for some worms, ELG-1 will be expressed during sequence pathway, therefore it will kill the HSN by apoptosis, leading to a c elegance that only produces sperm (male)
what is HSN?
-hemaphrodite specific neuron in c elegans
-serotonigernic neuron needed for laying eggs
what are the 2 mobile elements in th ETC?
-cytochrome c
-coenzyme Q
what is cytochrome c’s important function in vertebrate apoptosis?
release of cytochrome c from the mitochondria into the cytoplasm, and binding to APAF-1 triggers apoptosis
explain the apoptosis pathway in verterbrates?
what are the 2 different types of caspases? give ex for each
-initiator caspase: caspase 9
-effector caspase: caspase 3
whats the apoptosome?
huge complex composed of apaf 1 and cytochrome c
how does Bad work?
-it allows channel to form in the mitochondria, so that cytochrome c can get released into the cytoplasm
-it does this by freeing interaction between Bak and Bcl, which will allow Bak to go form a channel
-if Bad does not bind to Bcl, channel cant be formed and apoptosis cant happen
how do trophic factors control apoptosis in vertebrates?
-they keep bad in phosphorylated state, where it cant bind to Bcl
-trophic factors bind to trophic factor receptor, which then causes a phosphorylation cascade, leading to the phosphorylation of Bad
what are the different pro-apoptotic vs anti-apoptotic signals in nematodes vs mammals
what do cytotoxic t cells do?
-punch holes in membrane and activate caspases
-form special attachment cleft, and then secrete granules which contain stuff that punches holes in membranes and stuff that atcivates caspases
-perforin forms holes
-granzymes cleave bid, which recruits bax and bad, activate caspases
what do we mean by: trophic factors inhibit suicide, but death signals are assisted suicide
trophic factors can prevent cell from killing itself, but death signals can lead to the cell killing itself:
NK cell triggers apoptosis
cytotoxic t cells triggers apoptosis
