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BIOC212 > MVU12 INTRACELLULAR TRAFFICKING 3 AND 4 > Flashcards

MVU12 INTRACELLULAR TRAFFICKING 3 AND 4 Flashcards

1
Q

where do vesicles traffic?

A

between PM, early endoscope and trans Golgi network

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2
Q

what does the early endoscope mature into, and how does the membrane change?

A

matures into multi vesicular body (MVB) and the late endosome
membrane switches from Rab5 to Rab7

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3
Q

what does the late endosome mature into?

A

matures into the lysosome

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4
Q

what happens in the lysosome?

A

macromolecules are degraded to monomers

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5
Q

what are the tethers to endosomes?

A

Rab5 and CORVET

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6
Q

what are tethers to lysosomes?

A

Rab7 and HOPS

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7
Q

what do the tethers do?

A

bring vesicles close to endosomes

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8
Q

how does the membrane mature and switch from Rab5 to Rab7?

A

Rab5 at endosomes activates Rab7
Rab5 effector and tether (CORVET) is a GEF for Rab7
Rab7 effector is a GAP to inactivate Rab5
As Rab5 vesicles fuse with early endosome more and more Rab7 is activated and less and less Rab5 stays active
membrane becomes late ebdosome

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9
Q

how does the clustering of tethers happen?

A

Rab5 effectors have GEF or PI kinase activity on early endosome
GEF activity produces more Rab5-GTP in local area of membrane
PI-phosphates provide additional binding sites for vesicle tethers
cluster of tethers form landing site for vesicle
does not change membrane thickness or lipid content

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10
Q

what are SNARE proteins?

A

family of membrane proteins that carry out vesicle fusion

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11
Q

how does targeting and fusion happen?

A

rabs and tethers can recruit SNAREs to fusion site
v-SNARES on vesicles recognise partner t-SNAREs on target membranes
complexes form after tethering
unique combination of v and t-SNARES determine targeting specificity

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12
Q

what is the conformation of v-SNAREs?

A

monomers with single TM helical domain
not stably folded

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13
Q

what is the conformation of t-SNAREs?

A

trimers with combinations of TM and peripheral subunits
partially stable 3-helix bundle

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14
Q

what do v and t SNAREs form together?

A

a stable tetramer
4-helix bundle

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15
Q

what does the folding process of SNAREs do?

A

pulls membranes close together
generates physical string like a spring
not dependent on ATP or GTP

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16
Q

what is the fusion model?

A
  1. SNARE complexes form in a ring around the vesicle contact site
  2. the SNARE TM anchors are bent and strained, exerting a force that holds the membranes together
  3. the outer and inner layers of the membranes fuse
  4. the strain in the SNARE complex is relieved
17
Q

how does SNARE dissociation happen?

A

after fusion the SNARE complex is stable, unstrained and inactive
an AAA-family ATPase (NSF) dissociates v and t SNAREs, which are essential for the continuation of vesicle trafficking
t SNAREs become active again
v SNAREs are recycled back to their donor membrane by vesicles

18
Q

what does NSF do?

A

NSF binds SNARE complex through adaptor protein (alpha SNAP)
NSF twists and pulls during ATP hydrolysis
multiple cycles of ATPase unwind the SNARE helices

19
Q

what mediates endocytosis?

A

CCVs mediate endocytosis from PM to early endosome

20
Q

where are some PM proteins transported?

A

transported to recycling endosome, for exocytosis back to PM

21
Q

where are lysosomal proteins trafficked?

A

trafficked from trans-golgi to endosome, their receptors are trafficked brack

22
Q

how does receptor recycling work?

A

Extracellular ligands are bound by transmembrane PM receptors, transported to early endosome for sorting
pH of early endosome is lower than the extracellular space, causing ligands to separate from receptors
– changestheaveragecharge on proteins, interactions are weakened
Empty receptors are recycled back to PM
Free ligands progress to lysosome

23
Q

what is retrograde traffic and how does it work?

A
  • Retrograde traffic of proteins from endosomes to PM or trans-Golgi
    – extracellular receptors to PM
    – receptors that bring proteins to the
    lysosome are returned to Golgi
  • Involve membrane tubules or tubular vesicle, not round coated vesicles
  • Requires the Retromer protein complex
24
Q

how does endosome maturation happen?

A

Some TM proteins are marked for endocytosis by modification with mono-ubiquitin at PM
– not poly-ubiquitin
– recognition by CCV adaptors
– if ubiquitin is removed, proteins are
recycled to PM
– ubiquitin not removed is a signal for lysosomal degradation
* Early endosomes mature into MVBs by invaginating and pinching-off membrane
* MVB contents cannot be recycled to PM anymore

25
Q

how are MVB formed?

A
  • MVB invagination: a series of ESCRT protein complexes shape and pinch off vesicles into the lumen of an endosome
  • ESCRT-0 binds PI(3)P and collects mono-Ub cargo proteins, provides binding site for ESCRT-I
  • ESCRT-I and II form the neck of the bud
  • ESCRT-III forms oligomers to pinch off the bud to form vesicle
26
Q

what happens in the lysosome?

A
  • MVBs fuse with vesicles containing proteases and other enzymes to become lysosomes
  • After the ER, the lysosome is the final site of protein degradation in the secretory pathway
  • Lysosome lumen is highly acidic pH 5
    – normalproteinsunfold
    – lysosomalenzymesaremostactiveat low pH
  • Low pH is maintained by an ATP- dependent proton pump
  • Final breakdown products are returned to cytosol by small-molecule transporters
27
Q

what are the four paths for lysosome degradation?

A

endocytosis
phagocytosis
macropinocytosis
autophagy

28
Q

how does autophagy work?

A
  • Large-scale digestion of cytosol and membranes
  • Upregulated during starvation to release free amino acids
  • Lipids and proteins are transported through cytosol to form phagophore vesicle
  • Phagophore grows to enclose contents in an autophagosome
    – doublemembrane
    – largerangeofsizes
  • Autophagosome fuses with lysosome to digest contents
29
Q

how does homotypic fusion work?

A
  • In some fusion events, donor and target membranes are the same – fusionofCOP-IIvesiclesintovesicular-tubularclusterthat
    becomes cis-Golgi
    – re-formationofERandGolgiaftercelldivision
  • Both membranes have identical v- and t-SNAREs, already in
    complexes and inactive
  • SNAREs must be separated by NSF to allow new fusion
30
Q
A

BIOC212 (32 decks)

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