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cell bio cumulative > Intracellular support: MT, IF, and MF > Flashcards

Intracellular support: MT, IF, and MF Flashcards

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1
Q

What happens when the cytoskeleton or accessory proteins are getting damaged?

A

PATHOLOGIES: sickle cell anemia (MF), muscular dystrophy (MF), Alzheimers (MT), genetic skin blisters (IF)

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2
Q

Cytoskeleton Structure

A

internal support, balance between stable and dynamic

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3
Q

Cytoskeleton Function

A

organelle moving in a cell or cell moving in an environment.

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4
Q

Muscular Dystrophy(pathologies)

A

Microfilament
mutated dystrophin leads to poor organization and muscle dysfunction.
(dystrophin responsible for rectolinear pattern)

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5
Q

Sickle Cell Anemia(pathologies)

A

Microfilament
altered oxygen tension causing IRREVERSIBLE change in microfilament structure and irreversible sickle cells.

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6
Q

Alzheimers (pathologies)

A

microTuble function
dysfunctional Tau proteins

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7
Q

Genetic skin blisters (pathologies)

A

Intermediate Filament
mutation in IF leads to skin fragility

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8
Q

What are Microtubules used for?

A

Transport

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9
Q

What are Intermediate Filaments used for?

A

cell-cell communications but DO NOT CROSS THE CELL MEMBRANE

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10
Q

What are microfilaments used for?

A

membrane extension
MICROVILLI in small intestines are supported by microfilaments

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11
Q

What is a cytoskeletons stability, made up of, what is their function how are they modified?

A

have their protein polymers in a dynamic and interactive network.
they are static for support & dynamic for movement.
initiate, maintain, and REORGANIZE cell shape
made up of polymers
Polymers are modified by PTM

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12
Q

What features does Intracellular support have BOTH of?

A

cytoskeletal and cytomusculature

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13
Q

Similarities between MF, MT, and IF

A

polymers made from monomers
take part in cell support and/OR movement

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14
Q

Differences between MF,MT, and IF

A

diameter
stability
different types/roles of accessory proteins
1. control assembly
2. links filaments to each other
3. “motor proteins” moving fibers relative to each other.

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15
Q

Microfilaments
stability?
diameter?
occurence?
monomer type?
polymer type?
Polarity?

A

dynamic, easily assembled/disassembled
Narrowest filament
Monomer type: G-actin
polymer type: F-actin
polarity: polar bc made from g-actins which join head to tail

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16
Q

What is Microfilament polymerization dependent on?

A

ca++, ATP, monovalent ions, and accessory “formin” proteins.

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17
Q

What do we get from G-actin polymerization (F-actin)?

A

Filopodia and lamellipodia

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18
Q

What do lamellipodia and filopodia do?

A

wound healing (extension along the surface of the skin) or cancer(membrane extension can cause invasion of underlying tissue)

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19
Q

branched polymers drive what?

A

lamellipodia

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20
Q

bundled polymers drive what?

A

extension of filopodia. side by side bundled cross-linking proteins

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21
Q

How do we control microfilament structure AND function?

A

polymerization
accessory proteins: different kinds expressed at different levels in different cells.

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22
Q

accessory proteins for microfilament?

A

myosin motor proteins: cytomotility
kinASES: all phosphorylate but have different recognition abilities
Structural:
vinculin
talin
alpha-actinin

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23
Q

Which type of filament has two way communication?

A

Microfilament.
actin fibers, accessory proteins, integrins, extracellular proteins.

24
Q

What would happen if external function of integrins was changed? what would happen to internal function?

A

whatever happens on the outside happens on the inside, they have 2-way communication. Integrins are “linked on a chain”

25
Q

What can actin mediate?

A

mediates and can the release of viruses
example: HIV transport after entry depends on depolymerization

26
Q

How does HIV budding occur in a microfilament?

A

actin elongation

27
Q

What is the function of cytochalasin

A

goes with Microfilament.
Blocks elongation in actin which prevents the spread of HIV.
HOWEVER, cytokinesis and movement of healthy cells would be blocked too so it wouldn’t be able to work for HIV.

28
Q

How can we prevent the spread of HIV

A

we need to find a compound that is a good way to block the + end of actin.

29
Q

Intermediate Filaments
stability?
diameter?
occurence?
Polarity?

A

static
intermediate
cells subject to mechanical stress (skin) or long distances (nerves)
NOT POLAR- subunits are added or removed at the ends

30
Q

What are the four subclasses of Intermediate Filaments?

A

Keratin- skin, hair, nails, epithelia
vimentin- fibroblasts
neurofilaments- neurons
nuclear lamins- present in all cells that have a nucleus

31
Q

How are we going to make intermediate filaments disassemble?

A

phosphorylation

32
Q

How are we going to make intermediate filaments reassemble?

A

dephosphorylation

33
Q

WHEN do we need intermediate filaments to disassemble?

A

when we need mitosis- we dont want nuclear lamin
AND
cytokinesis- we dont want extensive IF network (its barrier to cell division)

34
Q

What are cell-cell connections made by?

A

desmosomes

35
Q

what are cell-substrate connections made by?

A

hemidesmosomes

36
Q

Why do you think intermediate filaments are polar?

A

because we need it to be stable to make long lasting connections

37
Q

What disease is associated with intermediate filament?

A

EBS- mutation in keratin IF nucleotide
one amino acid mistake causes cells to tear apart, blisters form, and the epidermis is lost

38
Q

How does a blister form?

A

cells lyse—> forms blister which causes the cells to die and we NEED WOUND HEALING.

39
Q

Microtubule
stability?
diameter?
occurence?
monomer?
polymerization?
Polarity?

A

dynamic, easy disassembled
widest
in all cells but in different amounts
they are the “highway” for motor proteins to move along
they are polar. (+ end, adding. - end, removing)

40
Q

What are the microtubule’s accessory proteins?

A

kinesins dyneins which provides intracellular motility. also, tau protein.

41
Q

what is the purpose of tau proteins?

A

facilitate assembly and control stability of microtubules
has low degree of phosphorylation which is good and NORMAL for healthy cell, that is how it stabilizes.

42
Q

what happens if we have excess tau proteins?

A

hyperphosphorylated tau–> not compatible for stability –> NEED depolymerization.

43
Q

What balances do we need to keep a cell normal?

A

control of assembly/disassembly
control of polymerization/depolymerization
control of phosphorylation/dephosphorylation

44
Q

microtubules in assembly/disassembly are involved in what?

A

chromosome separation/neuron axon. we need the balance of assembly/disassembly.

45
Q

what is katanin?

A

protein involved with Alzheimer’s

46
Q

In healthy cells, how much katanin is normal?

A

low amounts of phosphorylated tau. there is some depolymerization which is normal bc its balanced with polymerization.

47
Q

what happens if there is no balance in a microtubule?

A

there will be clumps of tau leading to alzheimers.

48
Q

when do we have high amounts of phosphorylated tau?

A

we have high amounts of katanin which means EXCESS MT depolymerization. NO BALANCE = UNHEALTHY= ALZHEIMERS.

49
Q

What are tubulin targetting drugs important in?

A

cancer chemotherapy

50
Q

What is taxol?

A

a microtubule cancer chemotherapy drug

51
Q

What is the function of taxol?

A

inhibits depolymerization
binds to and stabilizes the microtubule.
makes MT stuck in polymer form.

52
Q

Why is it important that taxol binds to and stabilizes the microtubule?

A

the microtubule will be stuck in their polymer form then it cant go through mitosis (chromosome separation).
THIS BLOCKS THE LATE STEPS.

53
Q

Why can’t we use taxol for alzheimers?

A

taxol cannot cross the BBB

54
Q

What do we use for alzheimers

A

EPOD because it can cross the BBB.
it still has some depolymerization but has MORE polymerization.
AXON TRANSPORT RESTORED CAUSING
causes better cognitive performance
EPOD was good in a mouse model.

55
Q

What is Colchicine, Colemid used for?

A

binds to monomer
prevents polymerization(contrast to taxol)
used for gout
decreases movement of WBC to areas w/uric acid.

56
Q

What is vinblastine, vincristine drug?

A

forms aggregates with monomers
prevents polymerization

progressive decrease in polymers bc depolymerization is still occuring, increase in monomers,

cell bio cumulative (3 decks)

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