COMPETITIVE EXAM MCQs SERIES of LIFE SCIENCES for CSIR-UGC NET/JRF, SLET, GATE, and other entrance tests: DEVELOPMENTAL BIOLOGY – Programmed Cell Death and Senescence.
Syllabus Outline
- Concepts and differences between apoptosis, necrosis, and autophagy.
- Key molecular regulators.
- Intrinsic (mitochondrial) and extrinsic (death receptor) apoptotic pathways.
- Role of p53 in apoptosis and DNA damage response.
- Cellular senescence: definition, telomere shortening, telomerase regulation and senescence pathways.
This quiz contains 25 concept-based, most frequently asked MCQs on “DEVELOPMENTAL BIOLOGY – Programmed Cell Death and Senescence”. Each question has a single correct/most appropriate answer.
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1. Cellular senescence is primarily defined as:
A) Temporary cell cycle arrest under stress
B) Irreversible growth arrest with metabolic activity
C) Rapid proliferation followed by differentiation
D) Programmed cell death via necrosis
2. Which of the following sequences correctly represents the steps involved in the extrinsic pathway of apoptosis?
A) Binding of a death ligand → Formation of the death-inducing signalling complex → Activation of caspase-8 → Activation of caspase-3
B) Binding of a death ligand → Release of cytochrome c → Activation of caspase-9 → Fragmentation of DNA
C) Binding of Fas ligand → Recruitment of Fas-associated death domain protein → Oligomerisation of Bax protein → Activation of caspase-3
D) Binding of tumour necrosis factor-alpha → Degradation of MDM2 protein → Activation of caspase-8 → Induction of autophagy
3. The “Hayflick Limit” refers to the observation that normal somatic cells can only divide a finite number of times. This limit is primarily dictated by:
A) The depletion of the mitochondrial pool.
B) The progressive shortening of telomeres to a critical length.
C) The accumulation of necrotic debris in the cytoplasm.
D) The activation of the extrinsic apoptotic pathway by growth factors.
4. What is the most likely long-term outcome of telomerase inhibition?
A) Inhibition of apoptosis leads to the ageing of the cell and reaches the Hayflick Limit faster.
B) Unrestricted proliferation leading to immortalisation.
C) Gradual shortening of telomeres leading to senescence.
D) Conversion to a necrotic phenotype due to energy depletion.
5. During early embryonic development, the removal of tissue between developing fingers or toes is an example of programmed cell death. Which of the following biochemical features best indicates this process in the interdigital tissue?
A) DNA is cleaved randomly, resulting in a smear pattern when analysed using agarose gel electrophoresis.
B) There is increased activity of mitochondrial respiratory complex IV along with high production of ATP.
C) DNA is cleaved at regular intervals between nucleosomes, resulting in a ladder-like pattern on an agarose gel.
D) The plasma membrane rapidly loses its integrity, causing leakage of lactate dehydrogenase into the surrounding extracellular space.
6. Consider a cell in which a mutation prevents the phosphorylation of the retinoblastoma protein. What would be the effect on the cell cycle?
A) The cell would progress through the S phase in an uncontrolled manner.
B) The cell would be permanently arrested in the G1 phase.
C) The cell would immediately undergo apoptosis.
D) The cell would enter a state of excessive proliferation and bypass senescence.
7. During the process of autophagy, what happens to the protein p62?
A) It is increased in amount to promote the formation of autophagosomes.
B) It moves to the mitochondria to trigger the release of cytochrome c.
C) It is degraded inside the autolysosome along with the material it carries.
D) It is secreted as part of the senescence-associated secretory phenotype.
8. The mitochondrial pathway of apoptosis is mainly controlled by the balance between which two groups of proteins?
A) Caspase-8 and Caspase-9
B) Telomerase and Shelterin complex
C) p53 protein and MDM2 protein
D) Pro-apoptotic and Anti-apoptotic
9. Which morphological feature distinguishes necrosis from apoptosis?
A) Presence of autophagosomes.
B) Maintenance of mitochondrial membrane potential.
C) DNA laddering.
D) Cellular swelling and rupture of the plasma membrane.
10. In a study on cellular senescence, a group of human fibroblast cells shows high levels of p16INK4a but low levels of p21. What is the most likely state of these cells?
A) They are in the early stage of cell cycle arrest caused by DNA damage.
B) They are re-entering the cell cycle after a temporary arrest.
C) They are undergoing rapid apoptosis.
D) They are in a stable and long-term senescent state.
11. Which of the following experimental observations would most clearly indicate that a cell is in the G1 phase of the cell cycle?
A) Formation of the pre-replicative complex along with high levels of Cyclin D
B) High levels of phosphorylated retinoblastoma protein and Cyclin B
C) A single sharp peak with the highest DNA content in a propidium iodide histogram
D) Presence of telomerase expression in the cytoplasm
12. What would be the effect of a mutation that inactivates the caspase-8 gene on a cell’s response to Fas ligand?
A) The cell would undergo apoptosis through the mitochondrial pathway.
B) The cell would show increased DNA fragmentation in a ladder pattern.
C) The cell would enter a state of senescence.
D) The cell would become resistant to apoptosis triggered by death receptors.
13. A mitochondrial protein “Z” induces phosphorylation of p53 at serine 46, promoting apoptosis. What is the most likely function of protein Z?
A) Anti-apoptotic protein
B) DNA damage response signalling protein
C) Telomerase complex component
D) E3 ubiquitin ligase for BAX
14. What is the expected effect of degrading all Inhibitor of Apoptosis Proteins in cells?
A) Increased resistance to apoptosis
B) Spontaneous apoptosis
C) Entry into resting phase (G0)
D) Increased telomerase activity
15. How does the drug rapamycin induce autophagy?
A) Phosphorylates LC3
B) Inhibits the mTOR complex
C) Activates p53 transcription
D) Damages mitochondria
16. Why does deletion of the CDKN2A locus delay cellular senescence?
A) Disrupts both p53 and Retinoblastoma pathways
B) Activates telomerase
C) Causes necrosis
D) Prevents DNA damage
17. What is the function of T-loop and D-loop structures in telomeres?
A) Attach chromosomes to the nuclear lamina
B) Enable telomeric RNA transcription
C) Accelerate DNA replication
D) Protect chromosome ends from DNA damage recognition
18. What does a shift from red to green fluorescence in JC-1 staining indicate?
A) Telomerase activation
B) Autophagy
C) DNA synthesis
D) Loss of mitochondrial membrane potential
19. Which protein directly inhibits initiator caspase-9?
A) X-linked Inhibitor of Apoptosis Protein
B) Bcl-2
C) SMAC
D) Fas ligand
20. Which statements correctly describe the role of p53 in cellular senescence?
I – p53 induces G1 arrest via p21
II – Continuous p53 activation is required for senescence
III – Senescence always requires telomere shortening
IV – p53 induces senescence in response to oncogene activation
A) I and II
B) I, II and IV
C) II and III
D) I and IV
21. Which of the following statements about telomerase is correct?
I – Telomerase is a ribonucleoprotein enzyme.
II – Telomerase contains its own RNA template, known as the telomerase RNA component.
III – The catalytic subunit of telomerase, called telomerase reverse transcriptase, functions as a reverse transcriptase.
IV – Telomerase adds repetitive DNA sequences to the 5′ end of the lagging strand.
A) I only
B) I and II
C) I, II and III
D) I, II, III and IV
22. Which effects are caused by telomere shortening?
I – Activation of DNA damage response
II – Stabilisation of p53
III – Induction of p21
IV – Reversible S-phase arrest
A) I, II, and III only
B) II and IV only
C) I and III only
D) I, II, III and IV
23. Which statement about the apoptosome is incorrect?
I – Composed of Bax, Bak, and cytochrome c
II – Requires ATP or dATP for assembly
III – Activates caspase-8
IV – Forms on mitochondrial membrane
A) I, II, III and IV
B) I, II and III
C) I, III and IV
D) II, III and IV
24. Assertion (A): Telomerase activity is necessary for the long-term survival of a species, but it is inactive in most somatic cells of long-lived mammals.
Reason (R): Although telomerase prevents replicative senescence, its inactivation in somatic cells helps suppress tumour formation by limiting the number of times a cell can divide and accumulate mutations.
A) Both A and R are true, and R correctly explains A.
B) Both A and R are true, but R does not correctly explain A.
C) A is true, but R is false.
D) A is false, but R is true.
25. Assertion (A): Sub-G1 peak analysis is more accurate than Annexin V/Propidium Iodide staining for apoptosis detection.
Reason (R): Sub-G1 measures DNA loss in fixed cells, whereas Annexin V/PI detects membrane changes in live cells.
A) Both true, and R explains A
B) Both true, but R does not explain A
C) A is false, but R is true
D) A is true, but R is false
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References
- Michael Barresi and Scott Gilbert (2023). Developmental Biology, Oxford University Press, 13th Edition.
- Lincoln Taiz, Ian Max Møller, Angus Murphy, and Eduardo Zeiger (2022). Plant Physiology and Development, Oxford University Press, 7th Edition.
- Geoffrey Cooper and Kenneth Adams (2022). The Cell: A Molecular Approach, Oxford University Press, 9th Edition.
- Alberts, B., Johnson, A., Lewis, J., Morgan, D., Raff, M., Roberts, K., & Walter, P. (2014). Molecular Biology of the Cell, Garland Science, 4th Edition.
- Robert A Weinberg, Robert A. Weinberg (2006). The Biology of Cancer, Taylor & Francis, 1st Edition.
- Gupta, P.K. (2022). Cell and Molecular Biology, Rastogi Publications, 5th Edition.
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