What gives cells their shape Flashcards
Microvilli (Actin-based structures)
Finger-like projections that increase surface area, aiding in absorption (e.g., in intestinal cells).
Built from bundled actin filaments, providing structural integrity.
Dynamic and capable of contraction to facilitate interactions with the extracellular environment.
Cilia (Microtubule-based structures)
Hair-like protrusions that facilitate movement and fluid flow (e.g., in respiratory tract).
Comprised of microtubule doublets arranged in a 9+2 pattern.
Movement is driven by dynein, a motor protein that generates bending forces.
Phagosomes (Actin-mediated phagocytosis)
Membrane-bound vesicles that engulf and digest particles.
Actin polymerisation drives the extension of the plasma membrane to form a phagosome.
Once internalised, phagosomes fuse with lysosomes for degradation.
How Phagosomes Work:
Phagocytosis begins at the plasma membrane – The cell extends actin-rich projections (pseudopodia) to surround and engulf a particle (e.g., bacteria, debris).
The engulfed particle is enclosed in a membrane-bound vesicle – This vesicle is called a phagosome.
Phagosomes move into the cytoplasm – They detach from the plasma membrane and travel inside the cell.
Fusion with lysosomes – The phagosome merges with a lysosome, forming a phagolysosome, where enzymes digest the engulfed material.
So, while phagosomes originate from the plasma membrane, they function inside the cytoplasm like lysosomes. Their role is to transport and degrade internalized material.
Actin Filaments
Actin is dynamic, undergoing rapid polymerisation and depolymerisation.
Forms networks that shape the cell, provide support, and drive cell motility.
Found in microvilli, filopodia, and lamellipodia, supporting cellular extensions and movement.
==> Highly dynamic: Actin monomers rapidly assemble and disassemble.
Composed of F-actin (filamentous actin) , which undergoes treadmilling (continuous polymerisation at the + end and depolymerisation at the - end).
Myosin motor proteins move along actin filaments, generating force for contraction, vesicle transport, and organelle positioning.
Microtubules
Function as the “highways” of the cell, enabling intracellular transport.
Govern the movement of organelles, vesicles, and chromosomes during division.
Key in cilia and flagella, providing a scaffold for their beating motion
Microtubules
Tubulin heterodimers (α- and β-tubulin) form hollow tubes.
Exhibit dynamic instability, constantly growing (+ end) and shrinking (- end).
Centrosomes act as microtubule-organising centres (MTOCs), determining cellular polarity.
G-actin vs. F-actin
G-actin (Globular actin): This is the monomer (single unit) form of actin.
F-actin (Filamentous actin): When multiple G-actin monomers polymerise, they form long, thin filaments (F-actin).
Treadmilling: G-actin monomers add to one end (+) and remove from the other (-), keeping actin filaments dynamic.
roles of actin and microtubules
Actin filaments directly interact with membrane structures, enabling:
- Phagocytosis: Actin pushes the membrane to engulf particles.
- Endocytosis/exocytosis: Actin assists in vesicle trafficking.
- Cell adhesion: Actin connects with integrins, enabling cells to anchor to surfaces.
Role of Microtubules in Intracellular Transport
Microtubules act as tracks for motor proteins:
- Kinesin moves cargo towards the plus-end (periphery).
- Dynein moves cargo towards the minus-end (centrosome).
Transport of organelles, granules, and vesicles is critical for cell function.
Microfilaments vs. Microtubules
Microfilaments = Actin filaments
Made of actin.
Thin and flexible.
Found mostly in the cell cortex (near the membrane).
Involved in cell movement, shape changes, and intracellular transport.
Examples: Microvilli, phagocytosis, and muscle contraction.
Microtubules
Made of tubulin.
Thicker and more rigid.
Act as the “highways” of the cell, moving cargo using motor proteins (kinesin & dynein).
Examples: Cilia, flagella, and mitotic spindles.
Are Microvilli Cilia?
No, microvilli and cilia are completely different!
microvilli
= increase SA for absorption
= actin based protrusions
cilia
= movement
= microtubule based (9+2)
cytoskeletal dysfunction in diseases (Ciliopathies_
Ciliopathies – Polycystic Kidney Disease (PKD)
What is it?
A genetic disorder caused by mutations in PC1 and PC2 (Polycystin-1 & Polycystin-2), which are proteins involved in ciliary function.
How does it affect the body?
Primary cilia are essential for sensing fluid flow and signaling within kidney cells.
When ciliary function is disrupted, kidney cells don’t get proper signals, leading to fluid-filled cysts in the kidney and liver.
This results in kidney dysfunction and enlarged kidneys over time.
How is the cytoskeleton involved?
Microtubules form the axoneme (core structure) of cilia.
Dynein and kinesin motor proteins transport cargo along microtubules in the cilia.
A malfunction in cilia structure or transport leads to ciliopathies like PKD.
cytoskeletal dysfunction in diseases (Cancer and the Cytoskeleton)
How does the cytoskeleton contribute to cancer progression?
Cancer cells remodel their actin cytoskeleton to migrate and invade tissues.
Steps of cancer spreading (metastasis):
ECM degradation: Cancer cells break down the extracellular matrix (ECM) to escape the tumor.
Intravasation: Cells enter the bloodstream.
Circulation: They travel through blood vessels.
Extravasation: They exit the bloodstream and invade new tissues.
Micrometastases form: Small clusters of cancer cells settle in new locations.
Colonization: The cells establish a secondary tumor by forming new blood vessels (angiogenesis).
Role of actin & microtubules in cancer:
Actin filaments help cancer cells migrate by forming lamellipodia and filopodia.
Microtubules assist in vesicle transport, cell division, and metastatic spread.
Targeting the cytoskeleton (e.g., using microtubule inhibitors like Taxol) is a common strategy in chemotherapy.
Summary
PKD is a ciliopathy caused by defective cilia (microtubule-based).
Cancer spreads due to cytoskeletal remodeling, mainly actin-driven migration and microtubule-supported transport.
