Cell death Flashcards
three ways a cell can die
apoptosis
autophagy
necrosis
Type 1 programmed cell death
apoptosis
stages of apoptosis simple
1) membran ebegins to blec
2) cell separates into membrane bound apoptotic bodies
3) cell shrinks
4) chromatin condenses
5) nuclear DNA fragments and organelles disintegrate
6) attracts macrophages to phagocytosse- cell content recycled
two pathways of apoptosis
intrinsic , extrinsic
which enzymes cause nuclear fragmentation
Casapse-3 cleaves ICAD, activating CAD
in the cell cycle, P53 detects DNA damage at the G1/S checkpoint and
triggers apoptosis- to stop the cell from becoming harmful and potentially cancerous
type 2 programmed cell death
autophagy
autophagy is characterised by
large vacuoles that eat any organelles before destruction of the nucleus
how is autphagy activated
by nutrient deprivation, neurodegenerative disease, stress, infection and cancer
stages of autophagy
1) isolation membrane formed
2) isolation mem collect unwanted cytoplasmic content
3) autophagosome forms
4) autoplysososme forms and degradation occurs - via acidicifaction
cytotoxic T cells express TCR that recognise seocfiic atnigens
e.g. cancerous cells- if the TCR is specific to it, it binds to its MHC 1 molecules and kills it
type 3 programmed cell death
necrosis
necrosis
trigged by external factors or disease
stages of necrosis
1) organelles swell
2) plasma membrane ruptures and autolysis occurs
3) releasing ROS- necrosis spreads
4) phagocytosis
difference between apoptosis and necrosis
1) apoptosis is triggere day normal processes in the body, whilst necrosis is triggered by external factors/ disease
2) apoptosis is beneficial, necrosis is abnormal nd harmful
3) in apoptosis organelles found in blebs, in necrosis organelles not found in blebs
4) in apoptosis cells splits into function apoptotic bodies, in necrosis, cell membrane ruptures releasing non function organelles
symptoms of apoptosis
no
symptoms of necrosis
inflammation and tissue death
wordy explanation of apoptosis
A cell is targeted, possibly due to DNA damage within the cell, or because of normal processes. Firstly, blebbing occurs and the cell starts to shrink. Furthermore, the nucleus and chromatin condense and nuclear fragmentation occurs. Secondly, apoptotic bodies form, containing functioning organelles. Finally, the apoptotic bodies are phagocytosed by neighbouring cells or macrophages.
two pathways of apoptosis
intrinsic extrinsic
- both activate caspases
Apoptosis - intrinsic pathway
mitochondrial
- development and homeostasis
extrinsic pathway
death receptors
- immune response- controlling cell numbers
Intrinsic pathway
1) cytosolic stress
2) translocation of pro-apoptotic BCL-2 family to mito
3) mito releases cytochrome C
4) recruits Cas9- activates Cas3
5) apptosis
Cas3
the executioner
Extrinsic pathway
1) FasL binds to Fas ont he death receptor
2) protein recruiting
3) death irncuign signal complex (DISC) formed
4) activating initiator Cas8
5) Cas8 activates Cas3/7
- -> executionors
factors which cause necorsis
toxins, trauma, hypoxia, ROS Cell damaged Influx of ca2+ ions Calpain activation Lysosome bursts Cathepsin (enzymes) released Cell death
3 types of autophagy
micro macro chaperone mediated Formation of an autophagosome Fusion to lysosomes = autophagolysosome Degradation via hydrolyses
autophagy occurs in response to
starvation, mTOR
autophagy is
caspase independent
