Introduction to Apoptosis Flashcards
(20 cards)
What is apoptosis?
A regulated form of cell death, ensuring controlled elimination without inflammation.
Where does the word apoptosis come from?
Greek: apo (from) + ptosis (falling) → “falling off,” like leaves from a tree in autumn.
How does apoptosis differ from necrosis?
Apoptosis → Cells shrink, contents remain enclosed, no inflammation.
Necrosis → Cells swell & burst, spilling contents → triggers immune response.
How much apoptosis occurs in humans daily?
50–70 billion cells die per day via apoptosis.
Why is apoptosis essential?
Maintains homeostasis – Prevents uncontrolled cell growth.
Inhibits cancer – Removes damaged/tumorigenic cells.
Supports proper development – Shapes organs/tissues in embryos.
What are examples of apoptosis in development?
Tadpole to frog – Tail regression during metamorphosis.
Digit formation – Webbed fingers removed before birth.
Neural pruning – Eliminates unnecessary brain neurons.
What can induce apoptosis?
Growth factor withdrawal.
DNA damage (e.g., sunburn response).
Cytoskeletal disruption by chemotherapy drugs.
ER dysfunction, oxidative stress, metal toxicity.
Immune attack (cytotoxic lymphocytes target infected cells).
Tumour suppression via p53 activation.
What happens if apoptosis is wrongly activated?
Excess apoptosis leads to tissue damage → Seen in heart attack or stroke (ischemia-reperfusion injury).
What are caspases?
A family of cysteine proteases, which cleave proteins C-terminal to aspartic acid residues.
How does caspase signalling work?
Caspase-9 (initiator) activates executioner caspases via proteolysis → amplifies the signal.
Executioner caspases cleave proteins → dismantles the cell internally.
Nucleases activated → Break chromatin into 200 bp fragments.
What experiment shows apoptosis’ effect on development?
Caspase-9 knockout mice → Excess neurons & webbed limbs, proving apoptosis regulates neural & limb formation.
Why was C. elegans important for studying apoptosis?
Every cell’s fate is known → 131 cells undergo apoptosis during development.
What are the key C. elegans apoptosis genes?
ced-3 & ced-4 → Required for apoptosis; loss-of-function leads to excess cells.
ced-9 → Inhibits apoptosis, similar to mammalian Bcl-2.
ced-4 is homologous to APAF-1, and ced-3 is related to caspases.
What are the two main apoptotic pathways?
Intrinsic (Mitochondrial) Pathway → Cytochrome C release from mitochondria triggers caspase activation.
Extrinsic (Death Receptor) Pathway → Fas receptors activate caspase-8 → engages mitochondrial apoptosis if needed.
How do Bcl-2 proteins regulate apoptosis?
Anti-apoptotic Bcl-2 proteins block apoptosis.
Pro-apoptotic Bcl-2 members (Bax & Bak) induce mitochondrial permeabilization.
Mitochondrial outer membrane permeabilization (MOMP) allows cytochrome C release, activating apoptosis.
How does the extrinsic pathway link to mitochondrial apoptosis?
Caspase-8 can activate Bid → Bid cleaves Bax/Bak → engages mitochondrial apoptosis.
What are signs of apoptosis?
Membrane blebbing → Phospholipid flipping.
Nuclear condensation → Chromatin shrinks.
Chromatin fragmentation → 200 bp nucleosome ladder.
Engulfment by neighbouring cells (phagocytosis).
How is apoptosis detected in labs?
TUNEL staining → Labels DNA breaks from nuclease activity.
What role does apoptosis play in brain development?
Excess neurons undergo apoptosis to refine connections.
Neurons deprived of growth factors (NGF, BDNF) die via apoptosis.
How can apoptosis contribute to neurodegenerative disease?
Abnormal activation in adult neurons leads to disorders like Alzheimer’s & Parkinson’s
