Vesicular Transport Flashcards Preview

BMS 242 - Advanced Cell and Molecular > Vesicular Transport > Flashcards

Flashcards in Vesicular Transport Deck (84)
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1
Q

What does endocytosis allow?

A

The capture of molecules from the outside of the compartment/cell

2
Q

What does exocytosis allow?

A

The secretion from compartment/cell to the outside

3
Q

What are the 3 main components in the plasma membrane?

A

Lipids
Carbohydrates
Proteins

4
Q

What do lipids contribute to the membrane?

A

Continuity and flexibility

5
Q

What do proteins contribute to the membrane?

A

Transport

6
Q

What do carboydrates contribute to the membrane?

A

Cell protection and tagging of cells

7
Q

Where are sugars present on the cell?

A

On the extracellular surface

8
Q

How are sugars attached to the cell?

A

To either lipids or proteins

9
Q

How do sugars protect the cell in damaging environments?

A

Forms a protective layer of the extracellular surface of the cell

10
Q

What is the structure of a phosopholipid?

A

Polar head group (hydrophillic) made of:
Amino acid (which can change)
Phosphate
Glycerol

2 hydrocarbon tails - one which has a cis-double bond to produce a kink

Ester bond between the glycerol and phosphate

11
Q

What are examples of phospholipids?

A

Phosphatidyl ethanolamine
Phosphatidyl serine
Phosphatidyl choline

12
Q

Which phospholipid is of net negative charge?

What does this mean?

A

Phosphatidyl serine

This phospholipid must be localised to the inside of the membrane

13
Q

What does phosphatidyl serine play a huge part in?

A

Cell function and cell death

14
Q

What is the difference between phospholipids and sphingolipids?

What is an example of a sphingolipid?

A

Sphingolipids have sphingosine instead of phosphate

Sphingomyelin

15
Q

What are needed to allow the membrane to be flexible?

Why?

A

Unsaturated fatty acids

Have a kink in there structure - providing disorder to the membrane

16
Q

What are unsaturated fatty acids?

A

Fatty acids which have a CIS double bond

Don’t have the maximum amount of hydrocarbons bound

17
Q

How many cis double bonds can be present in a hydrocarbon tail?

A

Many

18
Q

How many double bonds does Omega-3 have?

Omega-6?

A

3

6

19
Q

Where is Omega-3 produced?

What is it eaten by?

A

By sea plants

Eaten by fish

20
Q

Where is Omega-6 produced?

What is it eaten by?

A

By land plants

Eaten by land animals

21
Q

Why is it important to eat Omega-3 and Omega-6?

A

These cannot be made in the body

Must consume them to keep the membrane of cells flexible (they have many double bonds)

22
Q

What does cholesterol do in the membrane?

A

Helps to seal the porous plasma membrane and preserve internal molecules

Stabilises the membrane

23
Q

What is the structure of cholesterol?

A
  • 4 rings
  • Polar head group
  • Ridges hydrophobic tail
24
Q

What is the percentage of cholesterol in the membrane?

A

17%

25
Q

Which phospholipid has the highest percentage in the membrane and what is it?

A

Phosphatidyl choline

24%

26
Q

Which phospholipid has the lowest percentage in the membrane and what is it?

A

Phosphatidyl serine

4%

27
Q

How are intracellular molecule and vesicles kept away from each other and the plasma membrane?

A

They have negative charges

28
Q

What percentage of the inner leaflet is phosphatidylserine and why?

A

8%

Only found on the inner leaflet, due to its negative charge

29
Q

What does it mean if phosphatidylserine is exposed to the outside of the cell?

A

Signals that the cell is dying

Only occurs during apoptosis

30
Q

What does the exposure of phosphatidylserine to the outside of the cell label?

Why?

A

The dead cell and its remnants

So they are rapidly consumed by other cells

31
Q

What can phosphatidylserine flipover be detected by?

Where does this bind?

What colour is this?

A

Fluorescent Annexin V test

Binds to the heads of phosphatidyl serine

Red in colour

32
Q

What 2 things does vesicular transport allow?

A
  • Movement of material between distinct compartments of the cell
  • Movement to the outside environment
33
Q

What are transmembrane proteins?

What can the function of these proteins be?

A

Proteins which are inserted into the membrane

Ion channels/carriers/pumps

34
Q

What are peripheral proteins?

A

Proteins that are attached to one leaflet of the membrane through:

  • Lipid tails
  • Transmembrane proteins
35
Q

How is cholesterol transported into the cell?

A

By receptor-mediated endocytosis

36
Q

What carries cholesterol in he blood?

A

LDL (low-density lipoproteins)

37
Q

Describe the process of cholesterol into the cell

A

1) LDL binds to an LDL-receptor which has accumulated in a coated pit
2) ADAPTIN binds to the tails of the LDL receptors and recruits CLATHERIN
3) Clatherin coats the membrane and causes the membrane to invaginate
4) Coated pit forms a coated vesicle inside the cell
5) Coat dissasembles inside the cell - allowing the vesicle to fuse with the early endosome
6) Acidic environment of the early endosome causes LDL to dissociate from the LDL receptor
7) Receptor is recycles back to the plasma membrane in vesicles that bud off from the early endosome
8) Contents of the early endosoem is delivered to the lysosome, where the LDL proteins are digested

38
Q

Why is the early endosome important?

A

Receives ALL endocytosed material

39
Q

What type of molecule is adaptin?

A

An adaptor protein

40
Q

Why is there an acidic environment in the early endosome?

A

Protein pump - pumps protons in from the cytosol

41
Q

What is the environment of the lysosome?

A

Highly acidic with hydrolytic enzymes

42
Q

What does digesting the LDL protein in the lysosome cause?

A

Release of cholesterol, amino acids and small peptides into the cytosol

43
Q

What is cholesterol used for?

A

Synthesis of new membranes

44
Q

What do mutations in the LDL receptor result in?

Why?

A

Defective endocytosis
Leading to atherosclerosis (CVD)

Due to accumulation of lipoproteins in the blood and formation of plaques - blocking arteries

45
Q

How do mutations in the LDL receptor result in defective endocytosis?

A
  • Mutation in the tail
  • Can’t bind to adaptin
  • Coated pit cannot form
46
Q

What is the structure of clatherin?

A

Tri-legged and curved

47
Q

What does clatherin help with?

A

Membrane invagination, in order to form vesicles

48
Q

What molecules pinches the vesicles off from the planar cell membrane?

What does this molecule require in order to do this?

A

Dynamin

Requires GTP hydrolysis to produce energy

49
Q

What occurs when dynamin is mutated?

A
  • Defective endocytosis (vesicles cannot be pinched off

- Vesicles lie along the plasma membrane

50
Q

What do the ER and golgi use to pinch-off vesicles?

A

Clatherin-like coat proteins

51
Q

What Clatherin-like coat proteins is used to created vesicles from the golgi?

A

COPI

52
Q

What Clatherin-like coat proteins is used to created vesicles from the ER?

A

COPII

53
Q

Where is clatherin used from vesicle formation?

A

At the membrane and the early endosome

54
Q

What are newly synthesised proteins and lipids packages into?

What adaptor protein is used?

A

COPII vesicles

Sar1-GTP is the adaptor protein used

55
Q

What vesicle formation doesn’t require clatherin?

A

Phagocytosis

56
Q

What type of membrane invagination is required in phagocytosis?

How does this occur?

A

Actin-driven membrane invagination:

1) Microbe adheres to phagocyte
2) Phagocyte forms pseudopods that eventually engulfs the particle
3) Formation of a phagosome
4) Phagosome fuses with lysosome to form a phagolysosome
5) Microbe is killed and digested by lysosomal enzymes, leaving a residual body
6) Residual body is excreted from the cell and the useful material is released into the cytosome

57
Q

What is a phagocyte?

A

A cell which is capable of engulfing bacteria through phagocytosis

58
Q

What are pseudopods?

A

Temporary cytoplasmic projections

Created by actin

59
Q

What is a phagosome?

A

A phagocytic vesicle

60
Q

What are residual bodies?

How are they removed?

A

Vesicles containing indigestible materials

Secreted by the cell via exocytosis

61
Q

What is autophagy?

A

Elimination of malfunctioning cell elements

62
Q

How does autophagy occur?

A
  • Small vesicles fusing together around the disease organelle to form a continuous membrane (autophagosome)
  • Autophagosome then fuses to the lysosome
63
Q

How does fusion of vesicles to compartments occur when they are both intrinsically negatively charged?

A

Due to SNARE proteins

64
Q

How are membrane proteins transported from the ER?

A
  • Transport vesicles from the ER fuse to form transport intermediates
  • Transport intermediates move along microtubule tracts to the golgi
  • Membrane proteins leave the golgi in transport vesicles, which are delivered to the plasma membrane by microtubules
65
Q

What is exocytosis responsible for?

A

Secretion of:

  • Hormones
  • Digestive enzymes

Recycling of membrane receptors

Neuronal communication

66
Q

What are the 2 types of exocytosis?

A

Constitutive (all of the time)

Regulated (in response to a stimulus)

67
Q

Why must membranes come very close together in order to fuse?

A

Hydrophobic regions must interact and fuse

68
Q

What are v-SNAREs?

Example

A

SNAREs that are present on the vesicular membrane

Synaptobrevein (VAMP)

69
Q

What are t-SNAREs?

Examples

A

Target membrane SNARE

Syntaxin
SNAP25

70
Q

Which SNARE protein doesn’t have a transmembrane domain?

A

SNAP25

71
Q

What is formed on the initial contact between SNARE proteins and what does each SNARE contribute?

A

A tight 4-helical coiled coil

VAMP - one helice
Syntaxin - one helice
SNAP25 - 2 helices

72
Q

What forces the fusion of 2 compartments?

A

Coiling of the SNARE proteins in both membranes

73
Q

What happens to the SNARE coils post fusion?

What does this require

A

They are dissociated

Requires NSF with the help of:

  • Accessory proteins
  • ATP hydrolysis
74
Q

What does Botulinum neurotoxin do?

A

Attacks SNARE proteins

75
Q

What can botulinum and tetanus bacterial infections result in?

How?

A

Complete neuromuscular paralysis

By blocking exocytosis (important in Neuronal communication)
Blocks the release of Ach from presynapse to activate muscle contraction

76
Q

How can Botulism occur?

A

Through consumption of contaminated foods

77
Q

How can tetanus infection occur?

A

Dirty needles

Skin cuts

78
Q

What does BOTOX type A do?

A

Cleaves SNAP-25

79
Q

What does BOTOX type B do?

A

Synaptobrevin

80
Q

What does BOTOX type C do?

A

Syntaxin

81
Q

What is the mechanism of action of BOTOX?

A

1) Botulinum binds to the gangliosides on the presynaptic neuronal membranes
2) B enters the luminal space of recycling synaptic vesicles (endocytosed)
3) Following endocytosis - one subunit (SNARE protease) escapes the vesicle and cleaves specific SNARE protein
4) Cleaves SNARE can no longer support the fusion of synaptic vesicles - blocking neurotransmission for several months

82
Q

After infection with BOTOX, what leads to resumption of normal neuronal transmission?

A

Re-synthesis of the damaged protein

83
Q

What can BOTOX be used for medically?

How?

A

Local muscle paralysis:

  • Wrinkles
  • Muscle spasms

Injection with picogram amounts of BOTOX type A - cleaves SNAP-25

84
Q

How is SNARE peptidase released from BOTOX following endocytosis?

A

Vesicle is acidified - changing the structure of BOTOX and releasing the SNARE peptidase subunit