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MCB1 Block 3 > Exocytosis > Flashcards

Exocytosis Flashcards

1
Q

What is constitutive secretion?

A

A vesicle from golgi contains transmembrane and secretory proteins, and once it reaches plasma membrane it fuses and releases its proteins

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2
Q

What is regulated secretion?

A

a vesicle from golgi contains secretory proteins and once it reaches membrane it sits and waits - it doesn’t fuse until there is a signal to do so.

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3
Q

What is an example of something that uses regulated secretion?

A

Digestive enzymes, neurotransmitters

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4
Q

What is name for when a vesicle immediately fuses with the membrane/

A

constitutive secretion

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5
Q

What is the name for when a vesicle waits for a signal to fuse with the membrane?

A

Regulated secretion

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6
Q

What is a benefit of regulated secretion?

A

it allows for rapid secretion and a large amount of secretion at one time

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7
Q

What is a common signal for a vesicle in regulated secretion to fuse with the membrane?

A

calcium ion.

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8
Q

What prevents vesicle from immediately joining membrane in regulated secretion?

A

v-snare and t-snare start to connect, but do not fuse until there is a signal

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9
Q

When calcium is released via calcium ion channels into cytoplasm, what happens to vesicles waiting due to regulatory secretion?

A

The calcium binds to vesicles, allowing v-snare and t-snare to complete their interaction, and the vesicle fuses with the membrane

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10
Q

Polarized cells in constitutive secretion contain signals for what? (to tell them where on membrane to go)

A

apical vs. basolateral

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11
Q

Do unpolarized cells in constitutive secretion contain signals?

A

No

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12
Q

What is transcytosis?

A

combination of endocytosis and exocytosis.

Vesicle created on one end of cell, carried across and fusing with membrane @ opposite end of cell.

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13
Q

Describe how maternal IgG antibodies in breast milk are transported across intestinal epithelial cells

A

An infant who is breast feeding – milk goes into GI tract, antibodies (the variables are specific to specific antigen, the Fc region is constant region, the same for all antibodies). On epithelial cells there are Fc receptors (blue thing in picture) which bind to Fc portion of IgG antibody (so bind to all IgG antibodies), binding occurs @ low Ph of 6, endocytosis – to transcytosis (travels across cell) and then fuses with plasma membrane on opposite side, Fc receptor releases antibody b/c of higher pH. The receptor is recycled back to the opposite membrane to pick up more antibodies.

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14
Q

how is the mechanism for IgG antibody transcytosis in infants an exception?

A

Normally a receptor binds to a high pH and the low pH causes the release. the opposite is true for IgG

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15
Q

What pH is the intestinal lumen where the antibody binds to Fc receptor

A

6

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16
Q

What is the name of the receptor that binds to IgG?

A

Fc

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17
Q

What is the pH of the blood and interstitial fluid where the Fc releases IgG?

A

7

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18
Q

What happens to vesicles as they move across the golgi?

A

They decrease in size and increase in concentration

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19
Q

Why does the vesicle get smaller as it moves across the golgi?

A

for efficient exocytosis and to allow vesicle to get more acidic

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20
Q

How does a vesicle get more acidic as it moves across the golgi?

A

There is a hydrogen pump in the vesicle that pumps hydrogen ions into lumen, the longer the vesicle is there the more hydrogen will be pumped, the more acidic it becomes

21
Q

Why does the pH need to decrease in a vesicle?

A

So the cargo proteins will release the cargo

22
Q

What happens to the cargo receptor after vesicle secretes?

A

it is recycled with vesicle membrane back to trans golgi

23
Q

What is the “Pre” in a pre-pro-protein

A

the pre is an ER signal sequence that is cleaved off

24
Q

what is proalbumin the precuser of?

A

albumin

25
Q

What does the “pro” part mean in proalbumin

A

it has a propeptide domain

26
Q

How does proalbumin become active

A

The propeptide domain needs to be cleaved off

27
Q

Where does proalbumin become albumin?

A

in vesicle

28
Q

What regulates the initial docking & binding of v & t snares in exocytosis?

A

RAB-GTP

29
Q

What is the purpose of NSF/SNAPs?

A

they disentangle the v snare from t snare so that v snare can be recycled. they induce membrane fusion

30
Q

What is the name of the v-snare in the neuron?

A

synaptobrevin

31
Q

What is the name of the t-snare in the neuron?

A

syntaxin

32
Q

What signals the release of neurotransmitters?

A

Calcium

33
Q

What are the calcium triggered sensors in the neuron?

A

Synaptotagmins

34
Q

What is the name of the two things that form the fusion of the neuron to plasma membrane?

A

synaptobrevin (v-snare) and syntaxin (t-snare)

35
Q

What helps with the disassociation of synaptobrevin from synatxin in the neuron?

A

NSF

36
Q

key words: flaccid paralysis, synaptobrevin cleaved, ACh-stimulatory are linked to what disease?

A

Botulism

37
Q

Symptoms: Paralysis of respiratory and skeletal muscles (potentially fatal) because stimulatory NT is not released to elicit muscle contraction ! flaccid paralysis; “floppy baby syndrome” – hypotonia, hyporeflexia are what disease?

A

Botulism

38
Q

What causes botulism?

A

Botulin toxin

39
Q

What does the botulin toxin do to the neuron vesicles?

A

It cleaves the synaptobrevin (v-snare)

40
Q

What is the mechanism for botulism?

A

Cleaves synaptobrevin (V SNARE) of vesicles carrying ACh (stimulatory NT) → unable to interact with syntaxin → inhibits exocytosis/release of NT at NMJ

ACh cannot fuse with plasma membrane

41
Q

Key words: spastic paralysis, synaptobrevin cleaved, GABA&glycine-inhibitory, trismus, spatula test are what disease?

A

Tetanus

42
Q

symptoms: Prolonged contraction of skeletal muscles (potentially fatal), violent spastic paralysis; 1st sign – trismus (lock jaw), neck stiffness, dysphagia, pectoral & calf muscle rigity, muscle rigity & spasms; spatula test are what disease?

A

tetanus

43
Q

What causes the tetanus disease?

A

Tetanus toxin

44
Q

What does the tetanus toxin cleave?

A

synaptobrevin (v-snare)

45
Q

What is the mechanism for tetanus?

A

Cleaves synaptobrevin of vesicles carrying GABA & glycine (inhibitory NTs) → unable to interact with syntaxin → inhibits exocytosis/release of NT

46
Q

What is dysphagia?

A

Difficulty swallowing

47
Q

What is trismus?

A

lock jaw

48
Q

What is the first sign of tetnus?

A

lock jaw (trismus)

49
Q

What is the difference b/w the mechamisms of botulism and tetanus?

A

. In botuslism, its vesicles containing excitatory but tetanus is inhibitory NT.
In both cases it’s paralysis – but two different kinds.

MCB1 Block 3 (15 decks)

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