30 Advanced Part-C Style Questions (Cutin–Suberin–Waxes + Senescence–PCD)

Cutin–Suberin–Waxes (surface protection) और Senescence–PCD–HR response (cell death) को integrate करके मैं आपके लिए 30 CSIR-NET Part C level, medium-to-hard MCQs बना रहा हूँ। हर सवाल multiple concepts को जोड़कर होगा ताकि असली exam जैसा feel आए और आपको लगे कि आप actual paper solve कर रहे हैं

30 Advanced Part-C Style Questions (Cutin–Suberin–Waxes + Senescence–PCD)

Q1.

Consider the following statements:

1. Cutin is a macromolecule of ester-linked hydroxy/epoxy fatty acids.

2. Waxes are complex acyl lipids, most abundant as C25–C35 alkanes, alcohols, and aldehydes.

3. Suberin differs from cutin by having phenolic compounds and dicarboxylic acids.

4. Suberin deposition is typically associated with xylem differentiation.

Which statements are correct?

(A) 1, 2, 3 only

(B) 1, 2, 4 only

(C) 2, 3, 4 only

(D) 1, 2, 3, 4

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Q2.

Leaf senescence is promoted by:

1. Drought and mineral deficiency

2. UV-B and ozone

3. Darkness

4. Gibberellin accumulation

(A) 1, 2, 3 only

(B) 1, 2, 4 only

(C) 2, 3, 4 only

(D) All of the above

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Q3.

Vacuolar-type PCD requires:

1. Autophagy

2. Caspases

3. Metacaspases

4. Tonoplast rupture

(A) 1, 3, 4

(B) 2, 3, 4

(C) 1, 2, 4

(D) All 4

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Q4.

Which of the following are true about Hypersensitive Response (HR)-type PCD?

1. Earliest event is vacuolar swelling.

2. DNA degradation occurs.

3. Cell shrinks and contracts from cell wall.

4. Plasma membrane eventually ruptures releasing content into apoplast.

(A) 1, 2, 3

(B) 2, 3, 4

(C) 1, 4 only

(D) All of the above

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Q5.

Match the following protective layers with their characteristic functions:

i. Cutin

ii. Waxes

iii. Suberin

a. Prevents uncontrolled water loss at epidermis

b. Present in underground roots and wound-healing tissues

c. Highly hydrophobic acyl lipid mixture

(A) i-a, ii-c, iii-b

(B) i-b, ii-a, iii-c

(C) i-c, ii-b, iii-a

(D) i-a, ii-b, iii-c

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Q6.

Which one of the following is NOT a correct pair?

(A) Cutin → 16C, 18C hydroxy fatty acid esters

(B) Waxes → Mixture of alkanes, aldehydes, ketones

(C) Suberin → No phenolic component

(D) Cuticle waxes → Synthesized by epidermal cells

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Q7.

A plant under severe pathogen attack activates HR-type PCD. This process is adaptive because:

(A) It provides nutrients to pathogen

(B) It deprives pathogen of spreading nutrients

(C) It strengthens cuticle

(D) It reduces transpiration

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Q8.

Which of the following would most directly compromise barrier against pathogen entry?

(A) Mutation in cutin synthase

(B) Mutation in wax biosynthesis

(C) Mutation in suberin deposition

(D) All of the above

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Q9.

Necrosis differs from PCD in that:

(A) Necrosis is energy-dependent

(B) Necrosis is caused by physical/chemical damage

(C) Necrosis involves autophagy

(D) Necrosis is always developmentally programmed

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Q10.

During vacuolar PCD, which sequence of events is correct?

(A) Vacuole swelling → Tonoplast rupture → Hydrolase release → Cytoplasmic digestion

(B) Plasma membrane rupture → Vacuole swelling → Nuclear DNA degradation

(C) DNA degradation → Autophagy → Tonoplast rupture

(D) Nuclear DNA degradation → Cell wall lignification → Vacuole collapse

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Q11.

Which developmental process is NOT associated with vacuolar-type PCD?

(A) Xylem tracheary element differentiation

(B) Leaf morphogenesis

(C) Hypersensitive pathogen response

(D) Endosperm tissue digestion

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Q12.

If a mutation prevents lignification of secondary cell walls in xylem elements, vacuolar-type PCD will most likely:

(A) Leave cell wall intact

(B) Digest cell wall partially or completely

(C) Fail to initiate autophagy

(D) Fail to degrade organelles

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Q13.

Cutin and suberin both contain:

(A) Hydroxy/epoxy fatty acids with ester linkages

(B) Exclusively phenolic polymers

(C) Straight chain alkanes and aldehydes

(D) C25–C35 ketones as primary unit

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Q14.

Which stress is LEAST likely to trigger premature leaf senescence?

(A) Darkness

(B) Ozone

(C) Gibberellin

(D) High light

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Q15.

Senescence is distinct from necrosis because:

(A) Senescence is genetically regulated

(B) Senescence is energy-independent

(C) Necrosis is reversible

(D) Necrosis involves organ-level signaling

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Q16.

Which event is common to both HR-type PCD in plants and apoptosis in animals?

(A) Caspase activation

(B) Nuclear DNA degradation

(C) Tonoplast rupture

(D) Vacuolar swelling

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Q17.

Which of the following explains the protective function of cutin, waxes, and suberin?

(A) Restriction of water loss

(B) Barrier to microbial pathogens

(C) Structural rigidity

(D) A and B only

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Q18.

Abscission involves:

(A) Vacuolar-type PCD

(B) Separation of cell layers at leaf/fruit bases

(C) Necrosis of epidermal cells

(D) Secondary cell wall lignification

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Q19.

Which compounds are most abundant in cuticular wax?

(A) C10–C15 fatty acids

(B) C25–C35 alkanes and alcohols

(C) Phenolic lignin units

(D) Nucleic acid derivatives

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Q20.

A plant mutant defective in metacaspases would show impaired:

(A) Vacuolar-type PCD

(B) Necrosis

(C) HR-type PCD

(D) Senescence under stress

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Q21.

Which of the following are hallmarks of HR-type PCD?

1. Autolysis triggered by vacuole swelling

2. Cell shrinkage and contraction from cell wall

3. DNA degradation

4. Plasma membrane rupture

(A) 1, 2, 3

(B) 2, 3, 4

(C) 1, 3 only

(D) All 4

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Q22.

Which plant tissues typically contain high suberin content?

(A) Leaf epidermis

(B) Endodermis and periderm

(C) Pith cells

(D) Guard cells

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Q23.

Cutin is primarily composed of:

(A) Phenolics and polysaccharides

(B) Hydroxylated fatty acids crosslinked via ester bonds

(C) Sterol derivatives

(D) Polypeptide networks

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Q24.

Which is NOT an example of developmental PCD?

(A) Megasporogenesis

(B) Leaf senescence

(C) Pathogen-induced HR

(D) Tracheary element differentiation

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Q25.

Which event differentiates vacuolar-type PCD from HR-type PCD?

(A) Autophagy involvement

(B) DNA degradation

(C) Plasma membrane rupture

(D) Tonoplast rupture

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Q26.

If epidermal wax biosynthesis is inhibited, the most immediate physiological effect would be:

(A) Reduced secondary cell wall lignification

(B) Increased cuticular water loss

(C) Reduced pathogen entry

(D) Increased suberin deposition

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Q27.

A researcher observes that leaf cells shrink, DNA degrades, and cytoplasmic contents spill into apoplast during infection. Which process is occurring?

(A) Vacuolar PCD

(B) HR-type PCD

(C) Apoptosis

(D) Necrosis

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Q28.

Which of the following is an incorrect pair?

(A) Vacuolar PCD → Developmental

(B) HR-type PCD → Pathogen attack

(C) Necrosis → Genetically regulated

(D) Senescence → Environmental and genetic interaction

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Q29.

Which enzyme class is most essential in animal apoptosis but absent in plant PCD?

(A) Metacaspases

(B) Hydrolases

(C) Caspases

(D) Nucleases

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Q30.

Suberin differs structurally from cutin because it:

(A) Has no ester bonds

(B) Contains dicarboxylic acids and phenolic compounds

(C) Is mainly composed of alkanes

(D) Is exclusively synthesized by epidermal cells

✅ Answer Key with Explanations

Q1. → (A) 1, 2, 3 only

Suberin deposition is in underground/wounded tissues, not xylem directly.

Q2. → (A) 1, 2, 3 only

GA accumulation does not promote senescence.

Q3. → (A) 1, 3, 4

Metacaspases + autophagy + tonoplast rupture are essential; caspases are absent in plants.

Q4. → (B) 2, 3, 4

Vacuolar swelling is HR-excluded; instead shrinkage occurs.

Q5. → (A) i-a, ii-c, iii-b

Cutin = prevents water loss, waxes = hydrophobic acyls, suberin = underground barriers.

Q6. → (C)

Suberin does contain phenolics → so statement is wrong.

Q7. → (B)

HR-PCD deprives pathogen of nutrients.

Q8. → (D)

All 3 defects compromise defense.

Q9. → (B)

Necrosis = caused by physical/chemical injury.

Q10. → (A)

Correct sequence in vacuolar PCD.

Q11. → (C)

HR is not developmental but defense-driven.

Q12. → (B)

Without lignification, wall is digestible.

Q13. → (A)

Both cutin & suberin = hydroxy/epoxy FA ester-linked.

Q14. → (C)

GA delays senescence, not triggers.

Q15. → (A)

Senescence = energy-dependent + genetically programmed.

Q16. → (B)

DNA degradation common; caspases absent in plants.

Q17. → (D)

Main protective roles = A and B.

Q18. → (B)

Abscission = separation layer formation.

Q19. → (B)

Waxes have C25–C35 alkanes/alcohols.

Q20. → (A)

Metacaspases needed for vacuolar PCD.

Q21. → (B)

Shrinkage + DNA degradation + rupture; vacuolar swelling absent.

Q22. → (B)

Endodermis & periderm highly suberized.

Q23. → (B)

Cutin = hydroxylated fatty acid esters.

Q24. → (C)

HR is pathogen defense, not developmental.

Q25. → (D)

Tonoplast rupture is hallmark of vacuolar PCD.

Q26. → (B)

Cuticular wax defect → water loss ↑.

Q27. → (B)

That’s hallmark of HR-type PCD.

Q28. → (C)

Necrosis is NOT genetically regulated.

Q29. → (C)

Caspases are animal-specific, absent in plants.

Q30. → (B)

Suberin = ester-linked + dicarboxylic acids + phenolics.