Lecture 10 Flashcards
Describe the fluid mosaic model for membrane structure
Polar/ Hydrophilic heads
Nonpolar// hydrophobic tails
Lipid Rafts: rich in
a: cholesterol
b: glycophingolipids
c: sphingomyelin (sphingolipid)
Outer Leaflet: 1. phosphatidylcholine 2. sphingomyelin 3, phosphatidylethanolamine 4. glycosphingolipids. 5. glycolipid 6. glycoprotein
Inner Leaflet:
- phosphatidylethanolamine
- some phosphatidylcholine
- phosphatidylserine
- phosphatidylinositol
- PIP2
Discuss in general complex lipid (phospholipids and glycolipids) composition of the plasma membrane
Phospholipids: contain phosphate
Glycolipids: contain carb
Discuss the function of cholesterol in the plasma membrane
Note: cholesterol NOT found in intracellular membranes
Increase fluidity:
- inside bilayer
- lower temp (FA stiffer so prevents from stacking)
Decrease fluidity:
- polar head
- high temp: FA fluid and cholesterol ring slows it down
Discuss the factors involved in regulating membrane fluidity
Cholesterol not found in intracellular membranes
FA: determines fluidity Increase: 1. shorter FA 2. unsaturated FA esp arachidonic acid + docosahexaenic acid
Differentiate between active and passive transport systems based on energy requirement, and movement along the concentration gradient
Passive Transport: simple and facilitated diffusion
- with gradient
- no energy needed
- specific and saturable
- have maximal transport curve
Active Transport:
- Primary active: against gradient
- need ATP - Secondary active: against gradient
- use NA as co-transporter / exchanger
Discuss facilitated diffusion using the families of the glucose transporters GLUT 1-5 as examples and indicate their main locations and characteristics
Sodium-independent = facilitated diffusion
- GLUT 1: brain, RBC
- GLUT2: liver, kidney, intestine, B cells
- GLUT3: neurons
- GLUT4: muscle and fat; insulin dependent
- GLUT5: intestine, seminal vesicle. Likes fructose more
High affinity: 1, 3, 4
Low affinity: 2, 5
Describe the clinical features of hereditary GLUT-1 deficiency
Rare metabolic encephalopathy
- microcephaly
- epilepsy like seizures
Mature:
- ataxia
- delayed psychomotor development
- movement disorders
- impaired speech
Distinguish between primary active transport (Na+/K+ -ATPase) and secondary active transport (SGLT)
Secondary active transport system
- Na dependent
- uptake of glucose + galactose
- against gradient
1. SGLT-1 - symporter (Na + glucose + galactose = inside cell)
- against gradient
Primary Active Transport: - Na/K ATPase: 3 Na out 2 K in - cost: 1 ATP - against gradient
Explain the role of ABC transporters using CFTR as example
ABC: ATP binding cassette
- active transport (usually of lipids)
- against gradient
ie: CFTR (not a transporter but gated channel with Cl pore)
Cystic Fibrosis Transmembrane Conductance Regulator
CFTR DOES NOT pump Cl, its a with the gradient once channel is opened - passive diffusion (although few ATP cleaved)
Predict the effects of CFTR mutations in the lung epithelial cells and in the pancreas. Identify lab tests used for diagnosis of cystic fibrosis
Pancreas:
Makes enzymes and proteins that are meant to be released with water. If CFTR does not work, then won’t be releasing water and Cl.
Lung:
- Epithelial cell: Cl ions accumulate INSIDE cell so have higher conc inside than outside.
- Cl (negative ion) then is released with gradient OUTSIDE (extracellular lumen) along with water + Na
CFTR mutation in the secretory sweat gland:
CF baby with salty skin.
Sweat glands do not reuptake the Cl-
Labs: sweating induced to measure NaCl in the sweat
