Programmed Cell Death (Apoptosis)

33 questions • 2 tests • tap a section to begin

Welcome! Programmed Cell Death (Apoptosis) — 33 questions across 2 tests.

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  • Test 1 (7.2) — Programmed Cell Death (Apoptosis)
  • Test 2 (7.2) — Programmed Cell Death (Apoptosis)

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7.2 Programmed Cell Death — Test 1
Q1. Apoptosis is best described as:✓ A genetically programmed, regulated form of cell death
Q2. Which is NOT a morphological feature of an apoptotic cell?✓ Increased cell size
Q3. Regarding the plasma membrane in cell death:✓ It stays intact in apoptosis but ruptures in necrosis
Q4. Which statement about apoptosis is FALSE?✓ Cell contents are leaked into the surroundings
Q5. Apoptosis is executed by a family of proteases called:✓ Caspases
Q6. The two main apoptotic pathways are the:✓ Intrinsic (mitochondrial) and extrinsic (death-receptor) pathways
Q7. Which organelle initiates the intrinsic pathway of apoptosis?✓ Mitochondria
Q8. The death receptor that triggers the extrinsic pathway is:✓ Fas (CD95)
Q9. The initiator caspase of the extrinsic (death-receptor) pathway is:✓ Caspase-8
Q10. The initiator caspase of the intrinsic (mitochondrial) pathway is:✓ Caspase-9
Q11. The terminal (executioner) caspase common to both pathways is:✓ Caspase-3
Q12. The apoptosome is a complex consisting of:✓ Cytochrome c, APAF-1 and procaspase-9
Q13. A decrease in the BCL-2 / BAX ratio will:✓ Induce apoptosis
Q14. Which pair are both PRO-apoptotic?✓ BID and BAX
Q15. Among BCL-2, BCL-XL, A1 and BAX, which is NOT anti-apoptotic?✓ BAX
Q16. Bax and Bak promote apoptosis by:✓ Permeabilising the outer mitochondrial membrane to release cytochrome c
Q17. If cytochrome c is microinjected into a cell whose Bax and Bak are inactivated, the cell:✓ Still undergoes apoptosis (cytochrome c acts downstream of Bax/Bak)
7.2 Programmed Cell Death — Test 2
Q18. A peptide that disrupts mitochondrial membranes (releasing cytochrome c) would FAIL to cause apoptosis in cells that are:✓ APAF-1 mutated (no apoptosome can form)
Q19. In the extrinsic pathway, Fas ligand binding to Fas recruits which adaptor protein?✓ FADD
Q20. A drug that increases FasL, recruits FADD and cleaves caspase-8 (with p53 unchanged) acts via the:✓ Extrinsic pathway, independently of p53
Q21. Annexin V is used to detect apoptosis because it binds to:✓ Phosphatidylserine exposed on the outer membrane leaflet
Q22. In Annexin V / propidium iodide (PI) FACS analysis, EARLY apoptotic cells are:✓ Annexin V positive, PI negative
Q23. Which assay SPECIFICALLY detects apoptotic cells?✓ FITC-Annexin V based FACS analysis
Q24. Death-upon-detachment of anchorage-dependent cells from the matrix is called:✓ Anoikis
Q25. An inflammatory, lytic form of programmed cell death triggered by intracellular pathogens is:✓ Pyroptosis
Q26. Pyknosis during cell death refers to:✓ Nuclear collapse into a dense, condensed mass
Q27. Autophagy is carried out with the help of which organelle?✓ Lysosomes
Q28. Autophagosomes complete degradation by fusing with:✓ Lysosomes (forming autophagolysosomes)
Q29. How does autophagy relate to the DNA damage response?✓ It can promote cell survival in response to DNA damage
Q30. In a stress pathway, a transcription factor X is held inactive by inhibitor Y. If Y cannot be phosphorylated and degraded, then:✓ X stays cytosolic and apoptosis does NOT occur
Q31. In the same pathway, cells treated with Z-VAD-FMK (a pan-caspase inhibitor) will:✓ Fail to undergo apoptosis even if X reaches the nucleus
Q32. The synergy of BCL-2 with MYC in causing B-cell lymphoma shows that cancer often needs:✓ Both a block on apoptosis (BCL-2) and a drive to proliferate (MYC)
Q33. Overproduction of the anti-apoptotic protein BCL-2 contributes to cancer because it:✓ Allows inappropriate survival of cells that should die