8. Tissue Architecture Flashcards
Why might intermediate cytoskeletal filaments be resistant to stretching forces?
Because lateral contacts dominate in the organization of fibers, preventing stretching.
For intermediate filaments:
What do they do?
Where are they found?
Where are they anchored?
Enable cells to withstand mechanical stress (Great tensile strength)
Cytoplasm of most cells
Anchored to the plasma membrane at cell - cell junctions.
What configuration of protiens do you find in an intermediate filament?
8 staggered tetrameres form a region, which staggers to another 8 staggered tetrameric region in the growing strand.
In what disease might you find mutations affecting the basal lamina?
Progeria
What three structures do intermediate filaments make up in the cytoplasm of cells?
Keratin filaments
Vimentin (and vimentin-related) filaments
Neurofilaments
What role do intermediate filaments play in the nucleus?
They form the nuclear lamina
What roles to microtubules play in the cell?
They are vital to organization.
They form the mitotic spindle for chromosome segregation
They are part of cilia and flagella
On what end of a microtubule do you find gamma-tubulin?
The minus end
On which end of a microtubule might you see faster growth?
The plus end
What configuration of protiens makes up a microtubule?
Rings of alpha and beta tubulin stacked on top of each other.
What serves as the branching off point for microtubules at the centrosome?
Small rings of gamma-tubulin on the outside of the centrosome matrix
What stablizes microtubules at the distal end?
Microtubule capping protien
What does Taxol do?
Binds and stabilizes microtubules
Microtubules are like taxis for dynein. Taxol keeps those taxis going.
What four drugs mentioned in the slides bind tubulin dimers and prevent their polymerization?
Colchicine / Colcemid
Vinblastine / Vincristine
- Tubulin would like to get a job as a microtubule, but it can’t because of its CV*
- BLAST! CHRIST! I can’t get a job!*
For Microfilaments:
What are they made of?
What can help them become stable?
What do they do?
Fibrous F-Actin is made of a twisted polymer of G-Actin (globular actin)
They are often unstable unless associated with other protiens
They are associated with cell movements (locomotion, phagocytosis, cell division, contraction, etc)
What end of a Microfilament sees more growth?
The plus end.
What does Phalloidin do?
Where might it be found in nature?
What can it be used for?
Binds and stabilizes microfilaments (actin)
Deathcap Mushroom
Used in microscopy to stabilize actin for visualization
What does cytochalasin do?
What does latrunculin do?
Prevents the plus end of an actin filament from polymerizing.
Actin in the cell (cyto) gets heated (-chal) because it didn’t get the A+ (plus end)
Prevents actin monomers from polymerizing.
Keeps the lats from attaching to the trunk.
What are the basal laminae of cells made of?
Collagen
(Collagen IV and Laminin, primarily)
Note: In tutoring, we were expected to know what specific collagens did what. Creamer did not highlight that, or even present that, in his lectures.
What arrangement does collagen take?
Homo OR Hetero - dimer
Triple Helix
What triggers the self assembly of collagen?
Where is this collagen synthesized?
Where is it triggered to self assemble?
Cleavage of procollagen’s amino- and carboxy - terminal extentions.
In the cell
In the extracellular space
Note: the triple helix forms in the rough ER, but forming into fibrils and fibers happens in the extracellular space.
What disease is associated with a failure to hydroxylate collagen?
What causes this failure?
What are the main symptoms?
Scurvy
Lack of cofactor (vitamin C)
- Bleeding / opening of wounds
- Teeth falling out
For Ehlers-Danlos Syndrome
What is defective?
What happens as a result?
Collagen or collagen synthesis genes.
Skin is very stretchy, joints are hypermobile, bones, blood vessels, and organs can all be weaker.
For Adherens Junctions
What is the adhesion type?
What is the principal cell adhesion molecule (CAM) / adhesion receptor?
What is the cytoskeletal attachment?
What is the function?
Cell to Cell
Cadherins
Actin filaments
Shape, tension, singnaling, shearing force resistance
For Desmosomes
What is the adhesion type?
What is the principal cell adhesion molecule (CAM) / adhesion receptor?
What is the cytoskeletal attachment?
What is the function?
Cell - Cell
Desmosome Cadherens
Intermediate filaments
Strength, durability, signaling
For Hemidesmosomes
What is the adhesion type?
What is the principal cell adhesion molecule (CAM) / adhesion receptor?
What is the cytoskeletal attachment?
What is the function?
Cell - Matrix
Integrin (alpha6beta4)
Intermediate filaments
Shape, rigidity, signaling
For Tight Junctions
What is the adhesion type?
What is the principal cell adhesion molecule (CAM) / adhesion receptor?
What is the cytoskeletal attachment?
What is the function?
Cell to Cell
Occludin, claudin
Actin filaments
Controlling solute flow, signalling
For Gap Junctions
What is the adhesion type?
What is the principal cell adhesion molecule (CAM) / adhesion receptor?
What is the cytoskeletal attachment?
What is the function?
Cell to Cell
Connexins, innexins, pannexins
Attach via adapters to other junctions
Communication, small molecule transfer between cells
What is E Cadherin?
What is N Cadherin?
What is VE Cadherin?
What is LI Cadherin?
Which ones are typical vs atypical?
Epithelial cadherin
Neuronal cadherin
Vascular Endothelial cadherin
Liver-Intestine cadherin
All of these are typical except for liver-intestine, which is atypical
For all Cadherins
What do they work together to form?
What two junctions do they make?
What do they interact with?
Epithelial sheets
Adherens junctions and desmosomes
Other cadherins (homophilic) and actin in the cytoskeleton
What cadheren related phenominon do we see in transitional bladder cancer?
What does this change correspond with?
A decrease in E-cadherin and an increase in N-Cadherin
This change corresponds with an increase in invasiveness.
What is Epithelia to Mysenchymal Transition?
Change of cell shape from epithelial shape to a more mesenchymal shape in invasive cancer.
What is the special job of the Ig superfamily of CAMs?
What kind of binding are they capable of?
Interaction with immune cells
Both heterophilic and homophilic binding
What two main roles do selectins perform in immune response?
What are selectins dependent upon?
What increases presentation of selectins?
Assisting in rolling adhesion (low affinity slowing of leukocytes) and binding of extracellular carbohydrates
Calcium (they are calcium dependent glycoprotiens)
Local inflammation
What role do Integrins play in rolling adhesion?
They are the high affinity stops after selectins slow the leukocyte down. They use the beta2 family of integrins.
Other than rolling adhesion, what two other functions can Integrins perform?
They couple the extracellular matrix to the cytoskeleton using fibronectin, collagen, laminin, and vitronectin. (Aids in enduring pulling forces)
They can activate signalling pathways through interactions with receptor tyrosine kinase, which allows them to regulate growth, division, survival, differentiation, and apoptosis. (Everything we talked about last week)
