Cell & Developmental Bio - Plant Cells Lec 1,2,3

Q: Why is plant cell development critical for ecosystems and human industries?  

A: Plant-specific organelles like chloroplasts drive photosynthesis, sustaining ecosystems and oxygen production. Cell walls and vacuoles provide structural support and storage (e.g., starch in amyloplasts), underpinning agriculture (food, biofuels like Miscanthus grass) and pharmaceuticals (e.g., Plantago as a laxative, Calendula with anti-tumor properties). 

Q: What distinguishes primary and secondary plant cell walls?  

A:  

- Primary cell wall: Expandable, contains cellulose microfibrils linked by hemicellulose (e.g., xyloglucan) and embedded in a pectin matrix. Maintains cell adhesion via the middle lamella.  

- Secondary cell wall: Rigid, complex structures (e.g., lignin in wood) tailored for specialized functions (e.g., water transport in xylem).  

Q: How is cellulose utilized in industrial applications?  

A: Cellulose microfibrils (crystalline β-1,4-glucan chains) are used in paper, textiles, and nanofibers for drug delivery, hydrogels, and wound dressings. The forestry industry (worth ~$1 trillion) relies on cellulose for lumber and biofuels.  

Q: Describe the three major polysaccharides in plant cell walls.  

A:  

1. Cellulose: Scaffolding microfibrils (36 glucan chains, 5–12 nm wide).  

2. Hemicellulose (e.g., xyloglucan): Cross-links cellulose microfibrils.  

3. Pectin: Gel-like matrix in primary walls, rich in galacturonic acid, regulates cell adhesion and porosity.

Q: What roles do structural proteins play in the cell wall?  

A:  

- HRGPs (hydroxyproline-rich glycoproteins): Strengthen walls during stress.  

- PRPs (proline-rich proteins): Reinforce secondary walls.  

- GRPs (glycine-rich proteins): Provide flexibility and pathogen resistance.  

How do plants use cell walls to combat pathogens?  

A:  

- Callose deposition: Tomato plants deposit callose (β-1,3-glucan) at infection sites (e.g., Phytophthora infestans) to block pathogen entry.  

- Dynamic remodeling: Pathogens secrete enzymes to degrade walls (e.g., pectinases), but plants counter with inhibitors and structural reinforcements.  Q: How does turgor pressure drive plant cell growth?

A: Turgor (up to 20x car tire pressure) pushes the plasma membrane against the cell wall. Cellulose microfibrils direct expansion by resisting radial stretching, enabling directional growth (e.g., root elongation).

Q: How does turgor pressure drive plant cell growth?  

A: Turgor (up to 20x car tire pressure) pushes the plasma membrane against the cell wall. Cellulose microfibrils direct expansion by resisting radial stretching, enabling directional growth (e.g., root elongation).  

Q: Why is cell wall extensibility vital for plant development?  

A: Controlled loosening of the pectin matrix and hemicellulose crosslinks allows walls to expand. Enzymes like expansins disrupt hydrogen bonds, enabling cell enlargement during growth.  

Q: How do pathogens modify cell walls, and how do plants respond?

A: Pathogens secrete cellulases and pectinases to degrade walls. Plants retaliate with callose deposits, lignification, and protease inhibitors to block enzymatic activity.

Q: Describe the architecture of cellulose microfibrils in angiosperms.

A: Microfibrils consist of a crystalline core (24 glucan chains) coated with 12 amorphous chains, forming 36-chain assemblies (5–12 nm wide). This structure provides tensile strength while allowing interaction with water and glycans.

Q: Why is cell wall extensibility vital for plant development?

A: Controlled loosening of the pectin matrix and hemicellulose crosslinks allows walls to expand. Enzymes like expansins disrupt hydrogen bonds, enabling cell enlargement during growth.

Q: What is the role of the middle lamella?  

A: A pectin-rich layer that cements adjacent plant cells, maintaining tissue integrity. It is critical for cell adhesion in organs like leaves and fruits.  

Q: What physical barriers do plants use to prevent pathogen infection?

A: Plants employ trichomes (hair-like cell wall structures), thickened cuticles (waxy layers), and reinforced cell walls to block pathogen entry. For example, trichomes often lose their protoplasts during maturation, becoming purely cell wall-based barriers.

Q: How do plants detect pathogens early during infection?

A: Pattern Recognition Receptors (PRRs) on plant cells recognize Pathogen-Associated Molecular Patterns (PAMPs) (e.g., bacterial flagellin) and Damage-Associated Molecular Patterns (DAMPs) (e.g., cell wall fragments released during pathogen attack)

Q: What are the two layers of plant immunity?

A:

1. PAMP-Triggered Immunity (PTI): Initial defense via PRR-PAMP recognition, leading to ROS production and callose deposition.

2. Effector-Triggered Immunity (ETI): Stronger, targeted response triggered by pathogen effector proteins

Q: How does ROS contribute to plant defense?

A: ROS (e.g., hydrogen peroxide, H₂O₂) directly kills pathogens, crosslinks cell wall components to strengthen barriers (e.g., lignin formation), and acts as a signaling molecule to activate defense genes. Example: ROS production in Brachypodium distachyon during Magnaporthe oryzae infection.

Q: What is the role of callose in plant immunity?

A: Callose (β-1,3-glucan) forms papillae at infection sites (e.g., tomato leaves attacked by Phytophthora infestans), physically blocking pathogens and delivering antimicrobial compounds. It also signals downstream defense gene activation.

Q: How do pathogens modify plant cell walls to resist colonization?

A: Plants actively reinforce their cell walls to block pathogen invasion. Key modifications include:

1. Callose Deposition: β-1,3-glucan polymers form papillae at infection sites (e.g., tomato leaves attacked by Phytophthora infestans), physically blocking pathogen entry.

2. Lignification: Plants deposit lignin, a rigid polymer, to "armor" cell walls, making them impenetrable to enzymes like fungal cellulases.

3. Crosslinking: Reactive oxygen species (ROS) crosslink cell wall polysaccharides (e.g., pectin and glycoproteins), strengthening the wall structure.

4. Protein Reinforcement: Antimicrobial proteins (e.g., chitinases) and structural proteins like HRGPs (hydroxyproline-rich glycoproteins) are secreted to disrupt pathogen activity.

Q: How do pH changes in the cell wall benefit pathogens?

A: Pathogens alter pH to activate expansins (cell wall-loosening proteins) or deactivate plant defenses. For example, alkaline pH shifts can weaken pectin-Ca²⁺ bonds, facilitating tissue penetration.

Q: Why do pathogens target Ca²⁺ in the cell wall?

A: Ca²⁺ stabilizes pectin networks. Pathogens like Pseudomonas chelate Ca²⁺ to weaken walls, promote "gelification" of extracellular polymers (aiding adhesion), and suppress PTI signaling.

Q: How does turgor pressure relate to plant-pathogen interactions?

A: Pathogens reduce turgor pressure (e.g., via toxins) to collapse cells. Plants counteract by maintaining high solute concentration in vacuoles, preserving turgor to limit pathogen spread.

Q: How do plants reinforce cell walls post-infection?

A: Plants deposit lignin, suberin, and callose, and secrete antimicrobial proteins (e.g., chitinases). For example, tomato cells armor walls against Phytophthora by lignifying penetration sites.

Q: How do necrotrophs and biotrophs differ in modifying cell walls?

A:

• Necrotrophs (e.g., Sclerotinia) kill cells and secrete cellulases to degrade walls.

• Biotrophs (e.g., Blumeria) maintain host viability and use effectors to subtly manipulate wall structure.

Q: What are DAMPs, and how do they function?

A: Damage-Associated Molecular Patterns (DAMPs) are plant-derived signals (e.g., cell wall oligosaccharides) released during pathogen attack. They activate PRRs to amplify immune responses, such as ROS production.

Q: Summarize the "arms race" between plants and pathogens.

A: Plants evolve physical/chemical defenses (e.g., callose, ROS), while pathogens counter with wall-degrading enzymes, pH/Ca²⁺ manipulation, and effector proteins. Continuous adaptation drives co-evolution (e.g., Phytophthora vs. tomato).

Q: How do plants use Callose deposition to modify their cell walls to resist pathogen colonization?

Callose Deposition: β-1,3-glucan polymers form papillae at infection sites (e.g., tomato leaves attacked by Phytophthora infestans), physically blocking pathogen entry.

Q: How do plants use lignification to modify their cell walls to resist pathogen colonization?

Lignification: Plants deposit lignin, a rigid polymer, to "armor" cell walls, making them impenetrable to enzymes like fungal cellulases.

Q: How do plants use crosslinking to modify their cell walls to resist pathogen colonization?

Crosslinking: Reactive oxygen species (ROS) crosslink cell wall polysaccharides (e.g., pectin and glycoproteins), strengthening the wall structure.

Q: How do plants use protein reinforcement to modify their cell walls to resist pathogen colonization?

Protein Reinforcement: Antimicrobial proteins (e.g., chitinases) and structural proteins like HRGPs (hydroxyproline-rich glycoproteins) are secreted to disrupt pathogen activity.