Programmed Cell Death PCD
Introduction
- All living things are made up of cells. These cells are the building blocks of life.
- Every cell has a life cycle – it is born, works, and then dies in a proper order.
- When a cell dies in a planned and controlled way, it is called Programmed Cell Death (PCD).
- This process is like a “self-destruct button” inside the cell, which the cell uses when it is no longer needed or is harmful to the body.
- PCD is not random. It is a well-organized and natural part of growth and development.
- One clear example of PCD happens in human embryos (unborn babies).
- In early stages, the hands and feet of an embryo look like paddles, with no fingers or toes. But the cells between the fingers and toes die due to PCD.
- This helps in forming separate fingers and toes – that’s how we get 5 fingers and 5 toes.
- History
Origin and Types of Programmed Cell Death (PCD)
- The idea of Programmed Cell Death (PCD) was first introduced in 1964 by Lockshin and Williams while studying how insect tissues develop and break down.
- Later, scientists learned more about how PCD works by studying a protein called Bcl-2, which belongs to a group of related proteins found throughout evolution.
- The BCL2 protein is made by a gene that can cause cancer. This gene becomes active due to changes (called chromosome translocations) seen in a type of cancer called follicular lymphoma.
- BCL2 causes cancer by stopping the lymphoma cells from dying, which means they keep growing instead of breaking down.
- Bcl-2 family proteins control a process called MOMP (Mitochondrial Outer Membrane Permeabilization). These proteins are of two types:
- Pro-apoptotic (which help in cell death), like Bax, BAD, Bak, Bok
- Anti-apoptotic (which stop cell death), like Bcl-2, Bcl-xL, Bcl-w
- So far, scientists have discovered 25 different genes in the Bcl-2 family.
Types of Programmed Cell Death
- Apoptosis – This is called Type I cell death, where the cell dies in a clean and organized way.
- Autophagy – This is known as Type II cell death, where the cell breaks down its own parts to survive stress, but can also lead to death if it goes too far.
Apoptosis – A Type of Programmed Cell Death
- Apoptosis is a special kind of programmed cell death that takes place in multicellular organisms.
- During this process, many chemical changes happen inside the cell, which slowly change its shape and structure, eventually leading to its death.
- Some visible changes in a cell during apoptosis include:
- Blebbing (bubble-like bulges on the cell surface)
- Shrinking of the cell
- Breaking of the nucleus
- Condensation of chromatin (DNA becomes dense)
- Fragmentation of the DNA inside the nucleus
- Cells normally receive survival signals from their surroundings. If these signals stop, the cell may take it as a sign to self-destruct.
- Some studies also suggest that endonucleases (enzymes that cut DNA) may be responsible for triggering apoptosis.
- However, real apoptosis and programmed cell death are believed to be controlled by the cell’s genes—this means they are genetically regulated.
- It is also clear that mitosis (cell division) and apoptosis (cell death) are connected. The balance between them depends on signals that tell the cell whether to grow, divide, or die.
Autophagy – A Type of Programmed Cell Death
- Autophagy, also called Macroautophagy, is a process in which the cell breaks down and recycles its own parts.
- In this process, the cell forms a special structure called an autophagosome, which surrounds and captures:
- Large parts of the cytoplasm
- Damaged or extra organelles
- Abnormal protein clumps
- This autophagosome then fuses with a lysosome, which contains enzymes that digest these parts. This is known as autophagosomal-lysosomal degradation.
- Autophagy usually happens when the cell is lacking nutrients (starvation), so it reuses its own materials to survive.
- But it is also involved in many normal and disease-related processes, like:
- Growth and development
- Cell specialization (differentiation)
- Brain diseases (neurodegenerative disorders)
- Stress
- Infections
- Cancer
Other Types of Programmed Cell Death
Besides apoptosis and autophagy, scientists have discovered other types of programmed cell death (PCD). These types often act as backup systems when the main PCD pathways don’t work.
Some of the important types are:
- Necroptosis –
This is a non-apoptotic or caspase-independent type of programmed cell death.
It doesn’t use the enzymes (called caspases) used in apoptosis and often works as an alternative death pathway when apoptosis fails. - Anoikis –
It is very similar to apoptosis, but it happens when cells detach from their surroundings.
It prevents cells from surviving in the wrong place, which is important in stopping cancer spread. - Cornification –
This is a special type of cell death that occurs mainly in skin cells (not the eyes, as previously mentioned).
It helps form the outermost protective layer of skin and nails. - Excitotoxicity –
This happens when nerve cells get damaged or die due to excessive stimulation by certain chemicals like glutamate.
It is common in brain injuries and neurodegenerative diseases. - Ferroptosis –
This is an iron-dependent type of cell death. It happens due to oxidative damage and plays a role in cancer, brain diseases, and more. - Wallerian Degeneration –
This is a process where nerve fibers die back after injury.
It helps the body clean up damaged parts and sometimes allows nerve repair.
Atrophic Factors – Causes That Lead Cells to Die
Atrophic factors are natural conditions or forces that cause a cell to shrink, weaken, or die. These are not sudden injuries, but slow changes that reduce the cell’s activity or function over time.
Here are some common atrophic factors:
- Decreased Workload –
When a cell or tissue is not used for a long time (like a muscle after a bone fracture), it starts to shrink and weaken. - Loss of Nerve Supply (Innervation) –
If the nerve connection to a tissue is lost, the tissue may stop working and eventually die. - Reduced Blood Supply –
Without enough oxygen and nutrients from blood, the cells can’t survive. - Lack of Nutrients –
When there is a nutrient deficiency, cells can shrink and become inactive. - Loss of Hormonal Signals (Endocrine Stimulation) –
Some tissues need hormones to stay active. Without them, the tissues may atrophy (shrink). - Aging (Senility) –
As the body ages, cells naturally become weaker, leading to their death over time. - Compression (Pressure) –
Constant pressure on a tissue or organ can reduce blood flow and lead to cell damage or death.
Morphological and Physiological Changes During Apoptosis
When a cell goes through apoptosis (programmed cell death), many structural (morphological) and functional (physiological) changes take place.
Morphological (Structural) Changes:
- Apoptotic cells become small and dense – They shrink and look like tightly packed bodies.
- Chromatin (DNA material) breaks into pieces and is packed into membrane-bound small bodies along with some scattered cell organelles.
- The plasma membrane (outer covering of the cell) loses its normal shape and shows blebbing (bubble-like protrusions).
- Eventually, the cell breaks into smaller parts, called apoptotic bodies, each surrounded by a membrane.
- These apoptotic bodies show chemical changes on their surface, which help them get recognized and cleared by phagocytes (clean-up cells in the body).
Physiological (Functional) Changes:
- Macromolecule synthesis (like making proteins and RNA) is necessary before a cell can die in a programmed way.
- A special enzyme called endonuclease cuts the DNA at regular spots between nucleosomes (DNA packaging units).
- Calcium activates this enzyme.
- Zinc works as an inhibitor and stops the enzyme.
- The cell’s signal system (signal transduction) controls the flow of calcium (Ca²⁺) using specific receptors on the cell surface.
- The cell needs to make new RNA and proteins to carry out apoptosis.
- High levels of mRNA for degradative enzymes are made in the dying cells.
- Certain regulatory proteins control each step of the cell death process.
Genetic Level (Molecular Events):
- Scientists have found mammalian versions of ced genes (originally studied in roundworms) that control cell death.
- Many specific genes are involved in PCD.
- One such gene product is TRPM-2/SGP-2, which has been found in many unrelated cell death processes.
- During apoptosis, some genes like c-fos, c-myc, and heat shock proteins (70 kDa HSP) are activated one after another.
- These genes must stay in a demethylated (active) form to help the death process.
- Studies show that apoptosis is controlled (either turned on or off) by specific genes.
Molecular mechanism of programmed cell death
- Plant growth and development includes the degradation of cell organelles, protoplasts, different tissues and organs.
- It is a phenomenon to eliminate redundant, misplaced or damaged cells and maintain multicellular organisms.
- Apoptosis and plant programmed cell death have similarities like DNA laddering, caspase-like proteolytic activity in the cells and cytochrome c release from the mitochondria.
- Programmed cell death or apoptosis has an important role in animal development, metamorphosis, and tissue homeostasis.
- It is a genetically controlled physiological process that has two distinct and sequential processes: the death of cells, and their subsequent removal by engulfing cells.
A Cascade of Caspase Proteins
- Key insights into the molecular mechanism regulating cell death came from genetic studies in C. elegans.
- Of the 947 nongonadal cells generated during development of the adult hermaphrodite form, 131 cells undergo programmed cell death.
- Specific mutations have identified a variety of genes whose encoded proteins play an essential role in controlling PCD during C. elegans development.
- For instance, a PCD does not occur in worms carrying loss of function mutations in the ced-3 gene or the ced-4 gene, as a result the 131 “doomed” cells survive.
- CED-4 is a protease-activating factor that causes autocleavage of the CED-3 precursor protein creating an active CED-3 protease that initiates cell death.
- In contrast, in ced-9 mutants, all die during embryonic life, so the adult form never develops.
Three Classes of Proteins Function in the Apoptotic Pathway
- Key insights into the molecular mechanisms regulating cell death came from genetic studies in C. elegans.
- Scientists have traced the lineage of all the somatic cells in C. elegans from the fertilized egg to the mature worm simply by following the development of live worms under Nomarski optics. Of the 1090 somatic cells generated during development, 131 cells undergo programmed cell death.
- Specific mutations have identified a variety of genes whose encoded proteins play an essential role in controlling this process.
- For instance, in worms carrying mutations in the ced-3 or the ced-4 genes, programmed cell death does not occur, and all 1090 cells survive.
- In contrast, in ced-9 mutant animals, all 1090 cells die.
- These genetic studies indicate that the CED-3 and CED-4 proteins are required for cell death, that CED-9 suppresses apoptosis, and that the apoptotic pathway can be activated in all cells.
- Moreover, the finding that cell death does not occur in ced-9/ced-3 double mutants suggests that CED-9 acts upstream of CED-3 to suppress the apoptotic pathway.
- That apoptosis involved an evolutionarily conserved pathway was first suggested by the confluence of genetic studies in worms and studies on human cancer cells.
- The first apoptotic gene to be cloned, bcl-2, was isolated as a breakpoint rearrangement in human follicular lymphomas and was shown to act as an oncogene that promoted cell survival rather than cell proliferation.
- Not only are the Bcl-2 and CED-9 proteins homologous, but a bcl-2 transgene can block the extensive cell death found in ced-9 mutant worms.
- Thus both proteins act as regulators that suppress the apoptotic pathway.
- In addition, both proteins contain a single transmembrane domain and are localized to the outer mitochondrial, nuclear, and endoplasmic reticulum membranes.
- Three general types of proteins are critical in this conserved pathway.
- Regulators either promote or suppress apoptosis; the two regulators shown here, CED-9 and Bcl-2, both function to suppress apoptosis in the presence of trophic factors.
- Adapters interact with both regulators and effectors; in the absence of trophic factors, they promote activation of effectors.
- A family of cysteine proteases serve as effector proteins; their activation leads to degradation of various intracellular substrates and eventually cell death.
- The effector molecules in the apoptotic pathway are a family of enzymes called caspases, so named because they are cysteine proteases that selectively cleave proteins at sites just C-terminal to aspartate residues.
- These proteases have specific intracellular targets such as proteins of the nuclear lamina and cytoskeleton.
- Cleavage of these substrates leads to the demise of a cell.
- Activation of caspases, discussed below, appears to be a common feature of most, if not all, cell-death programs.
- The principal effector protease in C. elegans is CED-3. Mammalian cells contain multiple caspases.
- Cell-culture studies have yielded important insights into how the various CED proteins in C. elegans and the related mammalian proteins act together to control apoptosis.
- Expression of C. elegans CED-4 in a human kidney cell line induces rapid apoptosis. This can be blocked by coexpression of CED-9 (or mammalian Bcl-2).
- CED-9 directly binds to CED-4 and relocalizes it from the cytosol to intracellular membranes.
- Thus the pro-apoptotic function of CED-4 is directly suppressed by the anti-apoptotic function of CED-9. CED-4 also binds directly to CED-3 (and related mammalian caspases) and promotes activation of its protease activity.
- Biochemical studies have shown that CED-4 can simultaneously bind both to CED-9 and CED-3.
Pro-Apoptotic Regulators Promote Caspase Activation
• Having introduced the major participants in the apoptotic pathway, we now take a closer look at how the effector caspases are activated in mammalian cells. Although CED-9 and Bcl-2 suppress the cell-death pathway, other regulatory proteins act to promote apoptosis.
• The first pro-apoptotic regulator to be identified, named Bax, was found associated with Bcl-2 in extracts of cells expressing high levels of Bcl-2.
• Sequence analysis showed that Bax is similar in structure to CED-9 and Bcl-2, but overexpression of Bax causes cell death instead of preventing it, like CED-9 and Bcl-2 do.
• So, this family of related proteins includes both anti-apoptotic members (e.g., CED-9, Bcl-2) and pro-apoptotic members (e.g., Bax).
• All members of this family, known as the Bcl-2 family, are single-pass transmembrane proteins and can form complexes with each other.
• Whether a cell lives or dies may depend on which Bcl-2 family proteins are present and how they are controlled by cell signals.
• Recent studies show that Bcl-2 family proteins can affect where cytochrome c is located in the cell; also, cytochrome c helps activate caspases.
• In normal cells, cytochrome c is found between the inner and outer membranes of mitochondria, but in cells undergoing apoptosis, it moves into the cytosol.
• Bcl-2 overexpression can block this release of cytochrome c; on the other hand, Bax overexpression helps release cytochrome c into the cytosol and leads to apoptosis. In the cytosol, cytochrome c binds to the adapter protein Apaf-1 (mammalian CED-4), which starts a caspase cascade.
• Bax homodimers, but not Bcl-2 homodimers or Bcl-2/Bax heterodimers, allow ions to pass through the mitochondrial membrane.
• It is still not fully clear how this ion movement causes cytochrome c to be released.
The details of these pathways in any given cell type are not yet known.
(a) • In the absence of a trophic factor, Bad, a soluble pro-apoptotic protein, binds to the anti-apoptotic proteins Bcl-2 and Bcl-xl, which are located in the mitochondrial membrane.
• Bad binding stops these anti-apoptotic proteins from interacting with Bax, a membrane-bound pro-apoptotic protein.
• As a result, Bax forms homo-oligomeric channels (groups of Bax proteins) in the mitochondrial membrane, allowing ions to pass through.
• By an unknown process, this causes the release of cytochrome c from the space between the inner and outer mitochondrial membranes.
• Cytochrome c then binds to the adapter protein Apaf-1 (mammalian version of CED-4).
• This binding triggers a caspase cascade, which leads to cell death.
(b) • In the presence of a trophic factor such as NGF, in some cells, binding of trophic factors activates PI3 kinase, which then activates another kinase called Akt.
• Akt phosphorylates Bad, a pro-apoptotic protein.
• Phosphorylated Bad forms a complex with the 14-3-3 protein and stays in the cytosol.
• With Bad held in the cytosol, the anti-apoptotic proteins Bcl-2 and Bcl-xl are free to block Bax activity.
• This prevents the release of cytochrome c and stops activation of the caspase cascade, thereby preventing cell death.
• We saw earlier that neurotrophins like nerve growth factor (NGF) protect neurons from cell death.
• The exact intracellular signaling that links survival factors to the inactivation of cell-death machinery is not fully known, but some clues exist.
• It was found that trophic factors seem to act mostly without requiring new protein synthesis, which suggests that they act by modifying existing proteins.
• These modifications happen after translation (post-translationally), in response to signals triggered when trophic factors bind to their receptors.
• Studies showed that in the absence of trophic factors, nonphosphorylated Bad binds to Bcl-2/Bcl-xl at the mitochondrial membrane.
• This binding blocks the antiapoptotic action of Bcl-2/Bcl-xl and promotes cell death.
• When Bad is phosphorylated, it cannot bind to Bcl-2/Bcl-xl. Instead, it stays in the cytosol, bound to the 14-3-3 protein.
• Therefore, signaling pathways that phosphorylate Bad are strong candidates for delivering cell survival signals.
• Many trophic factors, including NGF, activate PI-3 kinase, which then activates Akt, a downstream kinase.
• Akt phosphorylates Bad at specific sites, which stops its pro-apoptotic activity.
• A special form of Akt that is always active (constitutively active) can rescue neurons that are deprived of neurotrophins and would otherwise die by apoptosis.
• These findings support the survival mechanism shown in Figure 2b.
• In other cell types, different trophic factors may promote survival by modifying other parts of the cell-death machinery after translation.
6. Programmed cell death in response to abiotic stress
• Plant cells and tissues are exposed to many abiotic stresses that can eventually cause their death.
• These stresses include toxins such as salinity, metals, herbicides, and pollutants (like reactive oxygen species [ROS]), as well as water shortage or excess, extreme temperatures, and strong light.
• Plants respond with adaptations that help them tolerate these conditions, remove toxins, or avoid extreme situations.
• Sometimes, abiotic stress causes stunted growth, and later, death of part or all of the plant.
• Cell death under stress may be a controlled process (PCD) that helps the plant survive.
• Or it may be uncontrolled death due to damage by harsh conditions.
• Programmed Cell Death (PCD) can be an adaptive response to help the plant survive stress.
• For example, plants in strong sunlight or low humidity may cover their surfaces with dead unicellular hairs.
• These cells die by PCD to form a protective layer that blocks light and traps moisture (Greenberg, 1996).
• Aerenchyma is a tissue with gas-filled spaces, found in roots of wetland plants and sometimes in dryland plants under stress.
• It can form naturally or in response to waterlogging.
• There are two types of aerenchyma:
- Lysigenous aerenchyma: formed when cells die and create air spaces (seen in rice, wheat, barley, maize) (Evans, 2004).
- Schizogenous aerenchyma: formed when gas spaces appear between cells during growth without cell death.
Seen in plants like Rumex and Sagittaria (Justin and Armstrong, 1987; Schussler and Longstreth, 1996).
• The plant hormone ethylene is involved in regulating cell death.
• In low oxygen (hypoxia) conditions, plants produce more ethylene (Jackson et al., 1985).
• In many species, ethylene can trigger the formation of aerenchyma.
• This shows that the cell death here is not mainly due to hypoxia but is a controlled process (Gunawardena et al., 2001).
• So, both abiotic stress and internal plant hormones can start cell death.
• In maize cells treated with ethylene or low oxygen, early signs of cell death include:
- Plasma membrane invagination,
- Denser cytoplasm,
- Membrane shrinking away from the cell wall (Gunawardena et al., 2001).
• Other signs include granular vacuole content and many vesicles under the membrane.
• Changes in the cell wall were also seen early in the death process.
• Nuclear condensation (a feature of apoptosis) was seen in S. lancifolia (Schussler and Longstreth, 2000).
• In animal cells, apoptosis involves apoptotic bodies—small, membrane-bound parts of the cell containing chromatin and organelles.
• Similar membrane-bound inclusions were seen in maize aerenchyma, but their function in plants is still unknown.
• They may protect organelles from breaking down, or help release enzymes that digest the cell wall and cytoplasm to form air spaces.
• Another feature of apoptosis is DNA fragmentation.
• TUNEL-positive nuclei (a sign of DNA fragmentation) were seen in maize root cortex forming aerenchyma due to ethylene and hypoxia (Gunawardena et al., 2001).
7. Programmed cell death in response to biotic stress
• Many studies have shown that PCD (Programmed Cell Death) is triggered in plants when they are attacked by pathogens, suggesting that PCD plays a central role in plant defense (Goodman and Novacky, 1994).
• Recent research has found that pathogen-infected plant cells actively begin a PCD process, triggered by specific host signals and requiring the production of new proteins or activation of specific pathways (He et al., 1994; Greenberg, 1997).
• There are two main types of cell death after a plant is infected:
1. Hypersensitive Response (HR) – A fast PCD process that stops the pathogen from spreading.
2. Disease symptoms – A slower form of cell death, caused by toxins from the pathogen. However, some mutants can show these symptoms even without a pathogen.
• HR is triggered when the plant detects a pathogen attack. Besides PCD, HR includes:
a. Oxidative burst,
b. Nitrosative burst,
c. Phytoalexin production,
d. Strengthening of cell walls,
e. Defense signals that act both locally and throughout the plant.
• Some phytotoxins (originally thought to damage the cell or block metabolism) are now known to trigger PCD actively (Navarre and Wolpert, 1999).
• Fungal toxins can both block metabolism and induce PCD (Stone et al., 2000).
• Phytoalexins, small secondary metabolites, are an important defense response. Their type depends on both the plant and the pathogen (Dixon et al., 1994).
• Phytoalexin biosynthesis occurs where the pathogen attacks, matching where PCD also happens (Dorey et al., 1997).
• Phytoalexins remain active even after cell death.
• The nature of signals that trigger PCD can help scientists find ways to control PCD.
• Several signal transduction pathways begin right after a plant detects a pathogen. These include:
- Calcium influx,
- Protein phosphorylation,
- Activation of phospholipases and G-proteins.
• These signals activate NADPH oxidase, leading to ROS (Reactive Oxygen Species) production.
• ROS can both trigger defense responses and PCD (Piffanelli et al., 1999; Hancock et al., 2001).
• When a plant recognizes a pathogen’s Avr gene, it triggers a signaling cascade that activates HR, ending in PCD.
• Key steps in HR are:
1. Avr gene interaction with the R gene (e.g., X1-RX1, X2-RX2),
2. Signal convergence into a common HR pathway,
3. NADPH oxidase activation to trigger PCD.
• Signals after NADPH oxidase are shared in almost all plant PCDs, including those triggered by development or abiotic stress.
• Other signaling molecules like calcium and salicylic acid (SA) also regulate NADPH oxidase and determine how much PCD and defense occur.
• When a plant recognizes a pathogen using its R gene, the signals must spread to the rest of the plant to trigger defense.
• Using kinase or phosphatase inhibitors, scientists found that protein phosphorylation/dephosphorylation plays a key role in defense.
• Several protein kinases involved in defense have been identified and cloned.
• Salicylic acid (SA) is a major signaling molecule in disease resistance, including PCD, and both local and systemic responses (Delaney et al., 1994).
• SA levels can increase 100-fold at the infection site.
• Applying external SA can activate defense genes, increase ROS, and induce PCD (Shirasu et al., 1997).
• Mutants with altered SA signaling often show changes in disease resistance.
• SA works together with other molecules like ROS, nitric oxide (NO), jasmonic acid (JA), ethylene, etc., making its specific role harder to define.
• SA effects include:
- Activating MAP kinase,
- Interacting with SA-response elements in gene promoters,
- Inhibiting mitochondria, showing SA is involved in many HR-related signals.
• Like SA, other hormones such as JA, ethylene, and abscisic acid (ABA) also influence defense and PCD (Dong et al., 1998; Klessig et al., 2000).
• These results mostly come from studies of hormone signaling mutants during pathogenesis and PCD.
MCQ
Q1. What is the full form of PCD?
A. Programmed Cell Death
B. Protein-Controlled Division
C. Partial Cell Decay
D. Pathogen Cell Deactivation
Answer: A. Programmed Cell Death
Q2. Programmed Cell Death (PCD) is also known as:
A. Accidental death of cells
B. Genetically controlled cell suicide
C. Unplanned breakdown of tissues
D. Necrosis
Answer: B. Genetically controlled cell suicide
Q3. Which of the following best describes the nature of PCD?
A. Random and uncontrolled
B. Always caused by infection
C. Organized and genetically regulated
D. Found only in animals
Answer: C. Organized and genetically regulated
Q4. What is a major visible example of PCD in human embryonic development?
A. Formation of lungs
B. Separation of fingers and toes
C. Eye formation
D. Growth of hair
Answer: B. Separation of fingers and toes
[PYQ – 2022, UOK Kota]
Q5. Which of the following is NOT a characteristic of PCD?
A. It is essential for development
B. It removes unwanted cells
C. It is always caused by disease
D. It involves genetic regulation
Answer: C. It is always caused by disease
Q6. Why is PCD referred to as a “self-destruct button”?
A. Because it triggers cell division
B. Because it spreads infection
C. Because it helps cells grow faster
D. Because cells destroy themselves when not needed
Answer: D. Because cells destroy themselves when not needed
Q7. Which term correctly refers to the life cycle of a cell?
A. Birth → Sleep → Division
B. Division → Mutation → Death
C. Birth → Work → Death
D. Synthesis → Mutation → Necrosis
Answer: C. Birth → Work → Death
Q8. In PCD, the decision for a cell to die is primarily:
A. External, due to viral attack
B. Random
C. A controlled internal mechanism
D. Because of nutrient abundance
Answer: C. A controlled internal mechanism
Q9. Which biological process is most closely related to the formation of paddle-like hands in early embryos?
A. Necrosis
B. Autophagy
C. Cell elongation
D. Programmed Cell Death
Answer: D. Programmed Cell Death
Q10. What happens to the cells between fingers during embryonic development?
A. They multiply rapidly
B. They become bones
C. They undergo PCD to form separate digits
D. They migrate to other parts
Answer: C. They undergo PCD to form separate digits
[PYQ – 2021, RRBMU Alwar]
Q11. Why is PCD important in multicellular organisms?
A. To increase disease resistance only
B. To maintain cell size only
C. For growth, development, and removal of unwanted cells
D. For nutrient absorption
Answer: C. For growth, development, and removal of unwanted cells
Q12. Who first introduced the concept of Programmed Cell Death (PCD)?
A. Watson and Crick
B. Lockshin and Williams
C. Avery and MacLeod
D. Hooke and Brown
Answer: B. Lockshin and Williams
[PYQ – 2019, M.Sc. Botany Entrance]
Q13. In which year was the term “Programmed Cell Death” introduced?
A. 1953
B. 1972
C. 1964
D. 1980
Answer: C. 1964
Q14. The study of which organism helped in the early understanding of PCD?
A. Mice
B. Insects
C. Bacteria
D. Yeast
Answer: B. Insects
Q15. Which protein family plays a key role in regulating PCD?
A. Tubulin family
B. Actin family
C. Bcl-2 family
D. Myosin family
Answer: C. Bcl-2 family
Q16. Bcl-2 is considered what type of protein in the context of PCD?
A. Pro-apoptotic
B. Anti-apoptotic
C. Stress-induced
D. Mutational protein
Answer: B. Anti-apoptotic
Q17. How does the Bcl-2 gene promote cancer?
A. By increasing cell division
B. By blocking DNA repair
C. By preventing cell death
D. By reducing cell metabolism
Answer: C. By preventing cell death
[PYQ – 2020, UOR Jaipur]
Q18. What is MOMP in the context of PCD?
A. A type of RNA
B. Mitochondrial Outer Membrane Permeabilization
C. A gene mutation
D. Cell cycle checkpoint
Answer: B. Mitochondrial Outer Membrane Permeabilization
Q19. Which of the following are pro-apoptotic proteins?
A. Bcl-2 and Bcl-xL
B. Bcl-w and Mcl-1
C. Bax and Bak
D. HSP70 and TRPM-2
Answer: C. Bax and Bak
Q20. Which of the following are anti-apoptotic proteins?
A. Bak and Bok
B. Bax and BAD
C. Bcl-2 and Bcl-xL
D. Apaf-1 and Caspase-9
Answer: C. Bcl-2 and Bcl-xL
Q21. How many genes approximately have been discovered in the Bcl-2 family so far?
A. 5
B. 10
C. 25
D. 50
Answer: C. 25
Q22. The role of Bcl-2 in follicular lymphoma is due to:
A. Chromosome translocation causing overexpression
B. Loss of tumor suppressor gene
C. Viral infection
D. Oxidative stress
Answer: A. Chromosome translocation causing overexpression
[PYQ – 2021, PDU Sikar]
Q23. Apoptosis is also known as:
A. Accidental cell death
B. Inflammatory death
C. Programmed cell death type I
D. Autophagy
Answer: C. Programmed cell death type I
[PYQ – 2022, UKU Uttarakhand]
Q24. Which of the following is NOT a characteristic feature of apoptosis?
A. Cell blebbing
B. Chromatin condensation
C. Cell swelling and bursting
D. Formation of apoptotic bodies
Answer: C. Cell swelling and bursting
Q25. What is the final stage in apoptosis?
A. DNA replication
B. Cell swelling
C. Formation of apoptotic bodies
D. Nuclear division
Answer: C. Formation of apoptotic bodies
Q26. Which enzyme is primarily responsible for DNA fragmentation during apoptosis?
A. Endonuclease
B. DNA polymerase
C. RNAase
D. Ligase
Answer: A. Endonuclease
Q27. Which event is not observed during apoptosis?
A. Chromatin condensation
B. Blebbing
C. Cell fusion
D. Nuclear fragmentation
Answer: C. Cell fusion
Q28. What triggers apoptosis when survival signals are absent?
A. Cell division signals
B. Hormonal stimulation
C. Cell starvation
D. Withdrawal of growth factors
Answer: D. Withdrawal of growth factors
[PYQ – 2020, Bhoj University]
Q29. Which of the following is a visible morphological change in a cell undergoing apoptosis?
A. Cell wall thickening
B. Cell shrinkage
C. Vacuole rupture
D. Cytoplasmic leakage
Answer: B. Cell shrinkage
Q30. Apoptosis is mainly regulated by:
A. Cell membrane proteins
B. Genetic signals
C. External viruses
D. Only temperature change
Answer: B. Genetic signals
Q31. The balance between mitosis and apoptosis is important for:
A. Promoting inflammation
B. Regulating gene expression
C. Maintaining tissue homeostasis
D. Enhancing viral replication
Answer: C. Maintaining tissue homeostasis
[PYQ – 2023, RGU UP]
Q32. Which of these best defines the process of blebbing?
A. Cell division by constriction
B. Release of enzymes from lysosomes
C. Formation of bubble-like projections on cell surface
D. Nuclear membrane disintegration
Answer: C. Formation of bubble-like projections on cell surface
Q33. What happens to DNA during apoptosis?
A. It becomes longer
B. It fuses with RNA
C. It fragments in an organized pattern
D. It is left untouched
Answer: C. It fragments in an organized pattern
Q34. Autophagy is also referred to as:
A. Type I cell death
B. Type II cell death
C. Necrosis
D. Hypersensitive response
Answer: B. Type II cell death
[PYQ – 2021, M.Sc. Entrance UOR]
Q35. The key structure involved in autophagy that engulfs cellular material is:
A. Ribosome
B. Nucleosome
C. Autophagosome
D. Endosome
Answer: C. Autophagosome
Q36. What does the autophagosome fuse with to degrade its contents?
A. Nucleus
B. Endoplasmic reticulum
C. Lysosome
D. Vacuole
Answer: C. Lysosome
Q37. Autophagy is mainly triggered by:
A. Overabundance of nutrients
B. Genetic mutation
C. Nutrient deficiency or starvation
D. Hormonal signaling
Answer: C. Nutrient deficiency or starvation
Q38. Which of the following is not a target of autophagy?
A. Damaged organelles
B. Abnormal protein clumps
C. Cytoplasmic material
D. Functional ribosomes
Answer: D. Functional ribosomes
Q39. Which cellular process is shared between both autophagy and apoptosis?
A. Lysosomal degradation
B. DNA synthesis
C. Protein translation
D. Controlled cell dismantling
Answer: D. Controlled cell dismantling
Q40. Autophagy is important during:
A. Organ formation
B. Cell fusion
C. Nutrient recycling and stress tolerance
D. Active cell division
Answer: C. Nutrient recycling and stress tolerance
Q41. What happens during autophagosomal-lysosomal degradation?
A. DNA is replicated
B. Cell becomes larger
C. Cellular waste is digested
D. Proteins are exported
Answer: C. Cellular waste is digested
Q42. Which of these conditions does NOT typically induce autophagy?
A. Oxidative stress
B. Starvation
C. Overnutrition
D. Low oxygen
Answer: C. Overnutrition
Q43. Autophagy helps plants and animals by:
A. Preventing cell growth
B. Enhancing random cell death
C. Recycling internal resources
D. Forming tumors
Answer: C. Recycling internal resources
[PYQ – 2020, UOK Kota]
Q44. In which of the following diseases is autophagy believed to play a significant role?
A. Hemophilia
B. Neurodegenerative disorders
C. Asthma
D. Typhoid
Answer: B. Neurodegenerative disorders
Q45. Which of the following is a caspase-independent programmed cell death?
A. Apoptosis
B. Necroptosis
C. Autophagy
D. Ferroptosis
Answer: B. Necroptosis
[PYQ – 2021, RRBMU Alwar]
Q46. Anoikis is a type of cell death that occurs when:
A. The cell bursts due to infection
B. The cell receives excess nutrition
C. The cell detaches from its surroundings
D. The DNA breaks randomly
Answer: C. The cell detaches from its surroundings
Q47. Which cell death process is essential in forming the outer protective skin layer?
A. Necrosis
B. Cornification
C. Excitotoxicity
D. Apoptosis
Answer: B. Cornification
Q48. Excitotoxicity is mainly observed in:
A. Skin
B. Liver
C. Heart
D. Nervous system
Answer: D. Nervous system
Q49. Which chemical is often involved in excitotoxicity leading to nerve cell death?
A. Histamine
B. Glutamate
C. Acetylcholine
D. Epinephrine
Answer: B. Glutamate
Q50. Ferroptosis is characterized by:
A. DNA mutations
B. Iron-dependent oxidative damage
C. Lysosomal breakdown
D. Calcium influx
Answer: B. Iron-dependent oxidative damage
[PYQ – 2023, UKU Uttarakhand]
Q51. Wallerian degeneration typically occurs after:
A. Viral infection
B. Genetic mutation
C. Nerve injury
D. Cell division
Answer: C. Nerve injury
Q52. The primary function of Wallerian degeneration is:
A. Immune cell activation
B. Removal of damaged nerve parts
C. Enhancing synapse formation
D. Preventing myelin production
Answer: B. Removal of damaged nerve parts
Q53. Cornification occurs mainly in which type of cells?
A. Neurons
B. Hepatocytes
C. Keratinocytes
D. Osteocytes
Answer: C. Keratinocytes
Q54. Which process is a defense against misplaced cells that could turn cancerous?
A. Necroptosis
B. Anoikis
C. Autophagy
D. Cornification
Answer: B. Anoikis
Q55. Which of the following is not a type of programmed cell death?
A. Apoptosis
B. Necrosis
C. Autophagy
D. Ferroptosis
Answer: B. Necrosis
[PYQ – 2018, M.Sc. Entrance]
Q56. What are atrophic factors?
A. Factors that increase cell division
B. Toxins causing acute cell lysis
C. Natural causes of slow cell shrinkage or death
D. Hormones that stimulate apoptosis
Answer: C. Natural causes of slow cell shrinkage or death
Q57. Which of the following is a common cause of cell atrophy?
A. Increased blood supply
B. Lack of use or workload
C. Overnutrition
D. Viral infection
Answer: B. Lack of use or workload
[PYQ – 2019, M.Sc. Entrance UOR]
Q58. What happens to a muscle that is not used for a long time?
A. Hypertrophy
B. Necrosis
C. Atrophy
D. Metaplasia
Answer: C. Atrophy
Q59. Loss of nerve supply to a tissue can result in:
A. Necrosis
B. Cell hyperplasia
C. Tissue growth
D. Atrophy
Answer: D. Atrophy
Q60. Which of the following can reduce blood supply to tissues, leading to atrophy?
A. Hormonal stimulation
B. Enhanced mitosis
C. Atherosclerosis
D. Excess oxygen
Answer: C. Atherosclerosis
Q61. Nutrient deficiency may lead to:
A. Apoptosis only
B. Cellular swelling
C. Cellular enlargement
D. Cell shrinkage and inactivity
Answer: D. Cell shrinkage and inactivity
Q62. Which hormone-related change can lead to atrophy?
A. Overstimulation by insulin
B. Loss of endocrine stimulation
C. Estrogen surge
D. Increase in growth hormone
Answer: B. Loss of endocrine stimulation
Q63. What is the natural process of tissue weakening due to aging called?
A. Senescence
B. Necrosis
C. Metaplasia
D. Hyperplasia
Answer: A. Senescence
[PYQ – 2020, PDU Sikar]
Q64. Which of the following best explains pressure-induced atrophy?
A. Tissue expansion due to cell proliferation
B. Compression leading to reduced blood flow
C. High temperature causing protein denaturation
D. Low pH affecting DNA replication
Answer: B. Compression leading to reduced blood flow
Q65. Which of the following is not an atrophic factor?
A. Loss of nerve supply
B. Aging
C. Increased workload
D. Nutrient deficiency
Answer: C. Increased workload
Q66. Which of the following statements about atrophy is correct?
A. It is always due to toxins
B. It is an accidental form of death
C. It helps the cell conserve energy during stress
D. It leads to immediate cell bursting
Answer: C. It helps the cell conserve energy during stress
Q67. What is a morphological change seen in apoptotic cells?
A. Cell enlargement
B. Cell swelling
C. Cell shrinkage and chromatin condensation
D. Cell wall breakdown
Answer: C. Cell shrinkage and chromatin condensation
[PYQ – 2022, RGU Uttar Pradesh]
Q68. Apoptotic bodies are:
A. Immune cells that remove dead cells
B. DNA fragments
C. Membrane-bound fragments of dying cells
D. Lysosomes
Answer: C. Membrane-bound fragments of dying cells
Q69. Which morphological feature is specific to apoptosis?
A. Blebbing
B. Lysis
C. Pyknosis
D. Osmotic rupture
Answer: A. Blebbing
Q70. What is the role of phagocytes in apoptosis?
A. To block apoptosis
B. To divide dying cells
C. To recognize and remove apoptotic bodies
D. To repair DNA
Answer: C. To recognize and remove apoptotic bodies
Q71. Which ion activates endonuclease involved in apoptosis?
A. Potassium
B. Sodium
C. Calcium
D. Magnesium
Answer: C. Calcium
Q72. Which ion acts as an inhibitor of endonuclease during apoptosis?
A. Calcium
B. Zinc
C. Sodium
D. Chloride
Answer: B. Zinc
Q73. What are nucleosomes?
A. DNA replication enzymes
B. DNA packaging units
C. RNA molecules
D. Cell organelles
Answer: B. DNA packaging units
Q74. Endonucleases cut DNA at:
A. Introns
B. Chromosomes randomly
C. Between nucleosomes
D. Centrosomes
Answer: C. Between nucleosomes
Q75. Which of the following is a physiological requirement for apoptosis?
A. Decreased ATP
B. Protein and RNA synthesis
C. Organelle multiplication
D. Glycolysis
Answer: B. Protein and RNA synthesis
Q76. Which of these is a sign of functional changes in a dying cell?
A. Protein synthesis stops before apoptosis
B. New RNA and proteins are made to support apoptosis
C. Enzymes stop working completely
D. DNA replicates rapidly
Answer: B. New RNA and proteins are made to support apoptosis
Q77. What happens to chromatin during apoptosis?
A. Becomes loose
B. Becomes more fluid
C. Condenses and fragments
D. Replicates
Answer: C. Condenses and fragments
Q78. Which gene was originally studied in roundworms (C. elegans) for its role in apoptosis?
A. Bcl-2
B. ced-3
C. ras
D. p53
Answer: B. ced-3
[PYQ – 2021, M.Sc. Entrance UOK]
Q79. The mammalian equivalent of the ced-3 gene is a:
A. Receptor protein
B. Caspase enzyme
C. Ligase enzyme
D. Histone protein
Answer: B. Caspase enzyme
Q80. Which gene in mammals is functionally similar to C. elegans ced-9?
A. Apaf-1
B. p53
C. Bcl-2
D. Ras
Answer: C. Bcl-2
Q81. What is the role of the TRPM-2/SGP-2 gene product in apoptosis?
A. Activates mitosis
B. Causes random DNA replication
C. Found in various cell death processes
D. Promotes cell survival
Answer: C. Found in various cell death processes
Q82. Which of the following genes is activated during apoptosis?
A. c-fos
B. actin
C. insulin
D. amylase
Answer: A. c-fos
[PYQ – 2020, UOK Kota]
Q83. What condition is required at the genetic level for apoptosis-related genes to function?
A. Methylated DNA
B. Mutation in promoter
C. Demethylated (active) state
D. Histone suppression
Answer: C. Demethylated (active) state
Q84. Which of the following is not a part of apoptosis regulation?
A. Bcl-2 family
B. Caspase family
C. TRPM-2
D. Amylase gene
Answer: D. Amylase gene
Q85. What is the main function of heat shock proteins (HSPs) in apoptosis?
A. Cell growth
B. DNA synthesis
C. Response to stress and regulating apoptosis
D. Glucose transport
Answer: C. Response to stress and regulating apoptosis
Q86. The gene Apaf-1 in mammals is similar in function to which gene in C. elegans?
A. ced-9
B. ced-4
C. ced-3
D. bcl-2
Answer: B. ced-4
Q87. Which of the following gene families is directly responsible for DNA fragmentation during apoptosis?
A. Polymerases
B. Caspases
C. Kinases
D. Ligases
Answer: B. Caspases
Q88. Apoptosis in cells is mainly regulated by:
A. Random injury
B. Membrane permeability
C. Gene-regulated molecular mechanisms
D. Physical breakage of nucleus
Answer: C. Gene-regulated molecular mechanisms
Q89. In C. elegans, how many nongonadal cells undergo programmed cell death during development?
A. 131
B. 947
C. 1090
D. 50
Answer: A. 131
[PYQ – 2022, RRBMU Alwar]
Q90. Which gene in C. elegans is essential for initiating apoptosis by activating proteases?
A. ced-9
B. ced-3
C. bcl-2
D. apaf-1
Answer: B. ced-3
Q91. Mutation in which C. elegans gene prevents apoptosis completely?
A. ced-3
B. ced-4
C. ced-9
D. Both A and B
Answer: D. Both A and B
[PYQ – 2021, M.Sc. Entrance UKU]
Q92. What happens in C. elegans when the ced-9 gene is mutated?
A. Only gonadal cells die
B. No cells die
C. All 1090 cells die during embryonic life
D. All cells survive
Answer: C. All 1090 cells die during embryonic life
Q93. What is the role of CED-4 in C. elegans?
A. Inhibits DNA synthesis
B. Activates CED-3 protease
C. Promotes cell division
D. Suppresses CED-9
Answer: B. Activates CED-3 protease
Q94. CED-9 suppresses apoptosis by:
A. Binding to apoptotic proteins
B. Preventing CED-4 activation
C. Degrading CED-3
D. Enhancing caspase transcription
Answer: B. Preventing CED-4 activation
Q95. In C. elegans, the gene ced-9 is functionally similar to which human gene?
A. Apaf-1
B. Caspase-9
C. Bcl-2
D. p53
Answer: C. Bcl-2
Q96. The proteins CED-3, CED-4, and CED-9 are involved in:
A. Mitosis
B. Protein synthesis
C. Cell death pathway
D. Photosynthesis
Answer: C. Cell death pathway
Q97. What is the effect of co-expressing CED-9 and CED-4 in human cells?
A. CED-9 enhances cell death
B. CED-4 is degraded
C. Apoptosis is blocked
D. DNA replication is stopped
Answer: C. Apoptosis is blocked
Q98. Which C. elegans protein directly binds both CED-9 and CED-3?
A. Caspase-3
B. Bcl-xL
C. CED-4
D. Apaf-1
Answer: C. CED-4
Q99. What experimental evidence supports that Bcl-2 suppresses apoptosis?
A. It increases CED-3 transcription
B. It blocks cytochrome c release in mammalian cells
C. It promotes cell proliferation
D. It inhibits MAP kinase
Answer: B. It blocks cytochrome c release in mammalian cells
Q100. What is the primary function of Bcl-2 in the apoptosis pathway?
A. Promote cell division
B. Inhibit apoptosis
C. Activate endonuclease
D. Enhance necrosis
Answer: B. Inhibit apoptosis
[PYQ – 2020, Bhoj University]
Q101. Bax protein promotes apoptosis by:
A. Inhibiting RNA synthesis
B. Blocking mitochondrial function
C. Releasing cytochrome c from mitochondria
D. Inhibiting CED-9
Answer: C. Releasing cytochrome c from mitochondria
Q102. Which family do Bax and Bcl-2 proteins belong to?
A. Caspase family
B. Bcl-2 family
C. Kinase family
D. G-protein family
Answer: B. Bcl-2 family
Q103. Cytochrome c is normally located:
A. In the cytoplasm
B. On the nucleus
C. Between inner and outer mitochondrial membranes
D. On the plasma membrane
Answer: C. Between inner and outer mitochondrial membranes
Q104. What does cytochrome c bind to in the cytosol to initiate caspase activation?
A. CED-3
B. CED-9
C. Apaf-1
D. Bax
Answer: C. Apaf-1
[PYQ – 2021, UOR Jaipur]
Q105. Which type of Bax complex allows ion movement in mitochondria?
A. Bax–Bcl-2 heterodimer
B. Bax homodimer
C. Bcl-2 homodimer
D. Bcl-2–Apaf-1 complex
Answer: B. Bax homodimer
Q106. What happens when Bad binds to Bcl-2 or Bcl-xL?
A. Apoptosis is suppressed
B. Caspases are deactivated
C. Apoptosis is promoted by preventing Bcl-2 function
D. Mitosis is initiated
Answer: C. Apoptosis is promoted by preventing Bcl-2 function
Q107. Which protein is responsible for phosphorylating Bad and preventing apoptosis?
A. Caspase-3
B. Apaf-1
C. Akt
D. Bax
Answer: C. Akt
[PYQ – 2018, M.Sc. Entrance UOK]
Q108. What is the role of the 14-3-3 protein in apoptosis regulation?
A. Stimulates Bax
B. Binds phosphorylated Bad and retains it in cytosol
C. Blocks cytochrome c
D. Activates caspase
Answer: B. Binds phosphorylated Bad and retains it in cytosol
Q109. Overexpression of Bcl-2 in mammalian cells:
A. Inhibits apoptosis
B. Causes DNA fragmentation
C. Enhances cytochrome c release
D. Triggers necrosis
Answer: A. Inhibits apoptosis
Q110. Which signaling pathway is mainly responsible for Bad phosphorylation and cell survival?
A. MAPK pathway
B. PI3-Kinase/Akt pathway
C. JAK/STAT pathway
D. TGF-β pathway
Answer: B. PI3-Kinase/Akt pathway
Q111. Which of the following abiotic stresses can induce programmed cell death in plants?
A. Salinity
B. Metal toxicity
C. Drought and heat
D. All of the above
Answer: D. All of the above
[PYQ – 2022, UKU Uttarakhand]
Q112. What is the role of unicellular hairs that die due to PCD in plants under sunlight or low humidity?
A. Help in seed dispersal
B. Protect against light and conserve moisture
C. Absorb nutrients
D. Attract insects
Answer: B. Protect against light and conserve moisture
Q113. Which type of aerenchyma is formed by cell death and air space creation?
A. Schizogenous
B. Chlorenchyma
C. Lysigenous
D. Collenchyma
Answer: C. Lysigenous
Q114. Aerenchyma formation in roots helps in:
A. Storing water
B. Floating in water
C. Facilitating gas exchange under waterlogged conditions
D. Absorbing minerals
Answer: C. Facilitating gas exchange under waterlogged conditions
[PYQ – 2021, PDU Sikar]
Q115. What is the role of ethylene in root cortex cells under hypoxic conditions?
A. Inhibits growth
B. Triggers random cell death
C. Triggers PCD and aerenchyma formation
D. Causes senescence
Answer: C. Triggers PCD and aerenchyma formation
Q116. Which of the following is not a typical cellular change observed during PCD induced by abiotic stress?
A. Dense cytoplasm
B. Plasma membrane invagination
C. Vacuole loss
D. Membrane detachment from cell wall
Answer: C. Vacuole loss
Q117. In maize cells under hypoxia, what nuclear change is seen during PCD?
A. Decondensation of chromatin
B. Enlargement of nucleolus
C. Chromatin condensation
D. Disappearance of nuclear envelope
Answer: C. Chromatin condensation
Q118. Which test is used to detect DNA fragmentation, a hallmark of apoptosis?
A. Western blot
B. ELISA
C. TUNEL assay
D. Bradford test
Answer: C. TUNEL assay
Q119. Which tissues in maize show TUNEL-positive nuclei during aerenchyma formation?
A. Root cortex
B. Leaf mesophyll
C. Shoot apex
D. Vascular bundle
Answer: A. Root cortex
Q120. What is the function of membrane-bound inclusions in PCD during aerenchyma formation?
A. Store calcium
B. Protect organelles or release enzymes
C. Regulate photosynthesis
D. Transport glucose
Answer: B. Protect organelles or release enzymes
Q121. In dryland and wetland plants, aerenchyma formation helps primarily in:
A. Increasing nitrogen uptake
B. Protecting from herbivores
C. Oxygen diffusion in submerged conditions
D. Pollination efficiency
Answer: C. Oxygen diffusion in submerged conditions
Q122. What type of programmed cell death is triggered rapidly at the site of pathogen attack in plants?
A. Autophagy
B. Necrosis
C. Hypersensitive Response (HR)
D. Ferroptosis
Answer: C. Hypersensitive Response (HR)
[PYQ – 2020, RGU]
Q123. The HR (Hypersensitive Response) in plants involves all of the following except:
A. Oxidative burst
B. Nitrosative burst
C. Apoplastic nutrient accumulation
D. Phytoalexin production
Answer: C. Apoplastic nutrient accumulation
Q124. What kind of phytotoxins are now known to actively trigger PCD in plant cells?
A. Insecticidal proteins
B. Necrosis-inducing toxins
C. Cell wall polysaccharides
D. Aquaporins
Answer: B. Necrosis-inducing toxins
Q125. Which secondary metabolites are produced in response to pathogen attack and PCD in plants?
A. Alkaloids
B. Phytoalexins
C. Terpenoids
D. Lignins
Answer: B. Phytoalexins
[PYQ – 2019, UOK Kota]
Q126. What is the main function of phytoalexins during biotic stress?
A. Promote DNA replication
B. Act as chemical defense molecules
C. Attract pollinators
D. Absorb excess water
Answer: B. Act as chemical defense molecules
Q127. Which enzyme is activated in plant cells during the oxidative burst phase of HR?
A. Catalase
B. NADPH oxidase
C. DNA polymerase
D. Lipase
Answer: B. NADPH oxidase
[PYQ – 2021, RRBMU Alwar]
Q128. The recognition of a pathogen’s Avr gene by a plant’s R gene leads to:
A. Chloroplast damage
B. HR activation and PCD
C. Flowering delay
D. Root elongation
Answer: B. HR activation and PCD
Q129. Which signaling molecules are involved in triggering ROS production during plant defense?
A. Calcium ions and G-proteins
B. Auxins and cytokinins
C. Gibberellins and abscisic acid
D. ATP and ADP
Answer: A. Calcium ions and G-proteins
Q130. Salicylic acid (SA) plays a central role in:
A. Cell elongation
B. Systemic acquired resistance and PCD
C. Nitrogen fixation
D. Water transport
Answer: B. Systemic acquired resistance and PCD
[PYQ – 2023, Bhoj University]
Q131. Which hormone, along with SA, modulates the extent of PCD during pathogenesis?
A. Ethylene
B. Cytokinin
C. Brassinosteroid
D. Auxin
Answer: A. Ethylene
Q132. Which kinase pathway is strongly activated by salicylic acid in plant defense signaling?
A. JAK-STAT
B. MAP Kinase
C. PI3K-Akt
D. TOR pathway
Answer: B. MAP Kinase