Cell Membranes/Junctions Flashcards
Exam 2
1
Q
What did Schleiden and Schwann do?
A
- Suggested there is a barrier between cells
1839
2
Q
What did Charles Ernest Overton do?
A
- Found that lipid soluble dyes penetrated cells, while others did not.
- So, determined the cell “barrier” was lipid-like
1895
3
Q
What did Irving Langmuir do?
A
- Langmuir trough looked at phospholipids
- Put phospholipids on a water surface. Then pushed device against phospholipids to measure pressure.
- Data showed that pressure would increase linearly, then dip, then resume increasing linearly.
- Dip is explained by phospholipids forming bilayer.
1917
4
Q
What did Gorter and Grendel do?
A
- Tried to determine if barrier was bi- or mono- layer.
- Extracted the phospholipids but didnt get all of them (under extracted).
- Then they wanted to figure out the total surface area (underestimated).
- The 2 mistakes canceled each other out and they determined that the surface area of the phospholipids were twice the surface area of the cell- so they determied it was a bilayer.
1925
5
Q
What did MUDD/MUDD do?
A
- found that RBCs in water-oil mix prefer oil, and WBCs in water-oil mix prefer water
- Determined they might be proteins w/ cell membranes
1931
6
Q
What happened in 1935?
A
- First model of cell membrane (Davcon-Danielli model)
- Appeared like sandwich (protein as bread, phospholipids as filling)
- Appeared like proteins formed distinct layers
7
Q
What did JD Robertson do?
A
- used an electron microscope to view the cell membrane
- Misinterpretd OsO4 for proteins- proposed glycoprotein coat
- Due to misinterpreting intercellular space as middle of sandwich
1950s
8
Q
1970s- Four experiments
Dan Braton and Freeze Fracture
A
- Did freeze-fracture and saw bumps on RBCs. Did freeze-fracture on liposome and saw no bumps. This indicated the bumps are significant.
- Inner leaflet (Protoplasmic/P-FACE, inside of monolayer closer to protoplasm) had more bumps
- Outer leaflet (inside of the monolayer cloer to extracellular space)
- the inner leaflet having more bumps shows proteins go through bilayer- implies mosaic model (many diff sized bumps)
first time integral membrane proteins (proteins that come through the membrane) came into the picture
9
Q
1970s - Four important experiements
Cell fusion
A
- human and mouse cell fused together
- Half the cell has human mAb w red flur marker, other half has mouse mAb with green flur marker, split perfectly down the middle
- monoclonal antibodies then mix around
- Conclusion: Integral membrane proteins can be fluid within the plan of the membrane
10
Q
1970s- Four important experiments
Cell capping/patching
A
- flur bivalent mAbs bound to membrane proteins- initially flur signal distributed uniformly across cell
- A second antibody that bound to the first was introduced which cross-linked the bound mAbs so they “capped” at one spot
- Same conclusion as cell fusion experiment (proteins are fluid in membrane), increasing its reliability
11
Q
1970s- four important experiements
FRAP
A
- Tags all integral membrane proteins with the same probe (Concanavalin A/ConA-carb binding protein)
- All proteins in cell membrane are glycosylated (have a carb attatched), so ConA binds to all glycosylated integral membrane proteins.
- Then, photobleach and watch recovery (FRAP). Showed only 50% of proteins hav free lateral mobility. Other 50% are stuck bc of collagen or microtubules
12
Q
What limits plasma membrane protein mobility?
A
- The cytoskeleton and extracellular matrix
13
Q
What did singer and nicholson do?
A
- proposed the fluid-mosaic model in 1972
14
Q
What is the difference between the fluid-mosaic model and the davson-danielli model?
A
- Fluid-mosaic includes transmembrane proteins (widely accepted, more accurate)
- DD model depicts protein as a separate layer on the surface (sandwich-incorrect)
15
Q
Why is the red blood cell membrane most studied?
A
- Plentiful and easy to collect
- Separated from WBCs easily- just from centrifuge
- No other membranes or organelles (only the cell membrane)
- Very few cell proteins. Makes the analysis of the proteins relatively simple.
- Can make your own red blood cell “ghosts” (resealed plasma membranes- can be resealed inside out or right side out)
RBCs is the first membrane that was approachable for us to figure out how the cell membrane proteins worked together
16
Q
What is hereditary spherocytosis?
A
- Mutation in membrane protein causes RBCs to be different shapes.
- Symptoms: anemia, jaundice, fatigue, splenomgaly
17
Q
What did Vernon Ingram do?
A
- “Father of molecular medicine” for his research on sickle cell anemia
- Most unrecognized scientist- he found the molecular difference that causes sickle cell anemia (only one amino acid difference!)
18
Q
What is the process for studying pure phospholipid bilayers?
A
- Treat with organic solvent- proteins and oligosaccarides form insoluble residue that is removed.
- Evaporate solvent
- Dissolve phospholipids in solvent and apply to small hole in partition
- now u have a liposome w pure phospholipid
19
Q
Studying pure phospholipid bilayers
Phospholipids
A
- Don’t do a lot and aren’t well studied
- Gases and small uncharged polar molecules are permeable
- Ions, charged polar molecules, and large uncharged polar molecules can’t permeate pure phospholipid bilayer
20
Q
Studying pure phospholipid bilayers
Phosphoglyerides
A
- Glycerol-based phospholipids
- Main comonent in the lipid bilayer
- ex. phosphatidylserine- only one that will flip flop from protoplasmic to ectoplasmic during apoptosis)
21
Q
Studying pure phospholipid bilayers
Sphingolipids
A
- chiefly in the cell membranes of brain and nervous tissue
- Ex. Sphingomyelin (on nerves). Wraps arround neurons to increase electrical resistance. Basis of many diseases including MS
