8 Membrane Trafficking Flashcards
*Q: What are 3 types of intracellular transport? Give examples for each.
A: gated transport eg nuclear import
Trans-membrane transport eg import of newly synthesised proteins into ER
Vesicular transport eg inter-organellar transport
*Q: Where are proteins made? Where do they then go? What happens here? 2 options?
A: RER where membrane bound polyribosomes make proteins (post translational mod)-> incorporated into vesicles -> cis GA-> medial GA -> trans GA ->
While passing through GA, undergo post translational mod
-> proteins sorted into specific transport vesicles ->
Those destined for cell surface membrane can enter 2 pathways:
1 -> constitutive secretory pathway
2 -> regulated secretory oath way
-> reach the cell surface membrane
(cell surface (via various secretory vesicle types))
*Q: Endocytosis overview.
A: material recognised at plasma membrane -> enter via endocytosis pathway -> early endosome = sorting compartment -> 3 options
- Recycling where material is sent back to the plasma membrane eg receptors
- Degradation
- Transcytosis where material is brought into the cell to be ejected on other side
Q: How are newly synthesised proteins directed to the compartment?
A: there’s a common pool of ribosomes that is used to synthesise proteins that stay in cytosol and those transported to ER- secreted and transmembrane
ER signal peptide (end terminal peptide) on a newly formed polypeptide will direct the engaged ribosomes to the ER membrane
At the end of each round of protein synthesis, ribosomal units are released and rejoin common poo, in cytosol
Q: What are examples of post translational modifications of proteins? (5) What happens at ER?
A: folding, forming disulphide bridges, glycosylation (adding sugars), proteolytic cleavages, assembly of multimeric proteins
At ER, if faulty, proteins are retained and exported back into cytosol where they’re degraded
Q: What is CF caused by in terms of the exocytosis pathway? What does the most common mutation lead to?
A: CFTR gene codes for CF transmembrane-conductance regulator
functions as = ABC transporter-class chloride channel in epithelial cell plasma membrane
Mutations is this affect functioning of chloride channels which causes CF
Most common mutation means misfolding which blocks ER exit -> therefore degraded in ER
Q: What occurs as proteins pass through the GA? (2) How is it organised?
A: the carbohydrate structure is modified where some sugars are removed and others added (glycosylation) via specific E
And at trans = sorted into vesicles to carry them to different destinations
Cis medial and trans where cis is closest to ER
Q: Differentiate between the 2 most common roots following exit of the GA.
A: 1 -> constitutive secretory pathway where there is a steady stream of vesicles from the trans-GA that fuse with the plasma membrane- exists in all cells to maintain cell membrane
(Unregulated)
2 -> regulated secretory pathway where proteins stored in secretory vesicles are released upon receiving a signal (such as a hormone) eg neurotransmitters in neurones
(Signalling molecule binds to cell surface receptor and triggers intracellular signalling pathways which causes release of stored secretory proteins)
Q: Apart from CF, give an example of a disease that is caused by a mutation resulting in ER retention.
A: SMED-SL = disease
Q: What are the 3 types of endocytosis?
A: receptor mediated- substances bind to specific receptors and begin to form a vesicle which has a protein coat around it
Pinocytosis- take in extra cellular fluid
Phagocytosis/ macropinocytosis- can take up large particles eg bacteria
Q: Provide an illustration of the degradation pathway of LDLs. Role? Recognition? (2) Result? (5) Recylcing.
A: LDLs that carry cholesterol and lipids to cells
Protein component LDLs is recognised by specific receptors on cell surface -> located in protein pits which invaginates and pinches off into cell to form clathrin-coated vesicles
(Pits containing receptors are covered in clathrin proteins)
Clathrin coating falls off to form uncharted vesicle-> fuses with early endosome
LDL from early endosome -> transferred to lysosomes -> degraded to produce free cholesterol
LDL receptors recycle back to the plasma membrane to be reused
Q: Give an example of a disease of endocytosis. Caused by?
A: familial hypercholesterolaemia
Caused by mutations in the LDL receptors
Q: How do vesicles move along in the cell?
A: move along cytoskeleton - motor proteins on microtubules
Q: How do lysosomes form?
A: lysosomal E are packaged into specific secretory vesicles with targeting signals specific to the lysosome after being tagged -> to late endosome -> environment is acidic which removes tag
Over time results in a late endosome which is full of lysosomal hydrolases -> matures to become lysosome
