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Block 4 Week 1 Dani > Muscle and Contractile proteins (BAKER) > Flashcards

Muscle and Contractile proteins (BAKER) Flashcards

1
Q

There are many myosin types with similiar (blank) but with differences in (blank) which correspond to differences in cargo and regulation.

A

motor domains

tails

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2
Q

Why type of myosin is associated with muscle myopathies?

A

type II

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3
Q

What type of myosin is associated with griscelli syndrome?

A

type V

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4
Q

What type of myosin is associated with hearing loss?

A

Type VI and VII

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5
Q

What is the function of myosin IIa?

A

involved in cell division

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6
Q

What is the function of myosin V?

A

involved in melanosome transport and certain neurological function

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7
Q

What is Griscellis syndrome and what causes it?

A

myosin Va point mtation leads to hypopigmentatiosn and neurological defects

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8
Q

What is the function of myosin VI and myosin VII and what is the disease associated with this?

A

maintains organization of actin-filled stereocilia

Mutations to myosin VI and VII associated with hearing loss. and usher syndrome (VII)

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9
Q

What is the structure of myosin II?

A

it is a dimer with motor domains and tails associated with heavy chains and 2 light chains (essential and regulatory)
with an active site and actin binding site

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10
Q

What is essential for myosin function?

A

coordination b/w actin binding site and active site

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11
Q

To generate ATP you need (blank) site.

A

actin binding site

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12
Q

all myosins are (blank) motors

A

actin-based motors

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13
Q

all but (blank) are plus-end directed myosin.

A

myosin VI

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14
Q

Actin is a long polymer structure, the polymer is (blank) allowing for directional muscle contraction.

A

polar

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15
Q

What are the sources of ATP in muscle and tell me the order that they are utilized.

A

ATP> creatinine>glycogen> lipolysis

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16
Q

with anaerobic respiration what do you get?

A

lactic acid and 2 ATPs

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17
Q

With aerobic respiration what do you get?

A

36 ATPs, CO2 and water and has myoglobin stores for oxygen

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18
Q

Why are aerobic cells red and what surrounds them?

A

aerobic cuz of myoglobin

vascularization surrounds it

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19
Q

Explain how muscle contraction works with actin and myosin

A

myosin is locked on actin in rigor configuration-> ATP binds and causes conformation on actin binding site->head displaces-> hydrolysis of ATP-> myosin binds to new site on actin filament-> release of phosphate-> power stroke and loss of ADP-> back to rigor state

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20
Q

Which has a bigger lever arm, myosin II or myosin V?

A

myosin V?

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21
Q

What is the mechanism of movement (working step) of actin and myosin?

A

lever arm otation

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22
Q

(blank) is a high (greater than 50%) duty ratio “processive” motor. i.e one head (motor) must be bound for 50% of its ATPase cycle

A

myosin V

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23
Q

(blank) transports vesicles in cells

A

myosin V

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24
Q

(blank) is a low duty ratio (less than 10%) motor

A

myosin II

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25
Q

What is this:
long neck (6IQ)
organelle motor
functional unit: two heads

A

myosin V

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26
Q

What is this:
shot neck (2IQ)
drives muscle contraction
functional unit: ~20 heads

A

myosin II

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27
Q

(blank) are far from processive

A

muscle myosin

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28
Q

How come some myosins can be processive and others cant/

A

the duty ratio tells us how long a myosin can hang onto an actin and if you have a very short duty ratio, then the myosin will just fall off and you cant processively (move like monkey bars).

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29
Q

How does muscle myosin (myosin II) contract?

A

by forming a thick filament with about 20 muscle heads and creates a successive contraction on actin

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30
Q

Many (blank) molecules are required to propel actin filament

A

myosin II molecules

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31
Q

In muscle, myosin II molecules are assembled into a (blank)

A

thick filament

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32
Q

(blank) form by association of hydrophobic regions in the tail.

A

filaments

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33
Q

(blank) is the fundamental contractile unit in muscle.

A

muscle sarcomere

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34
Q

The (blank) contracts when myosin thick filaments and actin thin filaments slide past each other.

A

sarcomere

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35
Q

(blank) and (blank)cap ends o actin to keep filament length constant.

A

CapZ and tropomodulin

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36
Q

(blank) contains alpha-actinin an other proteins that stably join sarcomeres.

A

Z disc

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37
Q

(blank) maintains thick filament position in the sarcomere.

A

Titin

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38
Q

(blank) sets the length of the thin filament

A

nebulin

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39
Q

What are the two types of muscle regulation?

A 
thin filament (skeletal and cardiac)
thick filament (smooth muscle)
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40
Q

Explain smooth muscle regulation?

A

phosphorylation= contraction

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41
Q

What activates myosin light chain kinase?

A

calcium-calmodulin

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42
Q

(blank) wraps around actin filaments blocking myosin binding sites on actin.

A

tropomyosin

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43
Q

(blank) binding to troponin C results in tropomyosin movement away from myosin binding sites.

A

calcium

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44
Q

The more calcium you add to the muscle, the more calcium that is bound to (blank) creating large powerstrokes.

A

troponin

45
Q

When looking at a graph of force and calcium, what does it tell us about the behavior of calcium in contraction?

A

it exhibits cooperativity

46
Q

Besides calcium, what else exhibits cooperativity?

A

myosin binding cuz it pushes troponin out of the way for the next myosin to attach

47
Q

What are 5 factors that affect muscles ability to generate force and to contract?

A 
myosin isoforms
frequency of stimulation
number of motor units stimulated
degree of stretch (frank-starling)
whether muscle is allowed to shorten (Force-velocity relationship)
48
Q

A complete muscle twitch is divided into what three phases?

A

latent, contraction, relaxation

49
Q

What is the latent period due to? So what does this mean?

A

AP, calcium

There is a delay between applied voltage and increase in tension

50
Q

What happens if you have a smaller time interval between contractions?

A

your second contraction will be bigger due to temporal summation of tensions

51
Q

What happens if you have continuous stimulation of a muscle?

A

temporal summation (as we apply more voltage, we get more stimulation, more release of calcium, stronger contraction), then we get tetanus (generating max force) and then fatigue (decreased tension)

52
Q

Asynchronous motor unit activity maintains a nearly (blank) in the total muscle

A

constant tension

53
Q

A motor neuron and all of the muscle cells it stimulated is called a (blank)

A

motor unit

54
Q

If we activate more than one motor neuron via an interneuron, what will our force be like?

A

increased due to recruitment

55
Q

The strength of a muscle contraction is determined not only by the frequency of stimulation but also by the (blank and blank) of motor units recruited

A

number and size

56
Q

In vivo, the number of motor units that are recruited is determined by the number of (blank) that are stimulated by the central nervous system

A

motor neurons

57
Q

In addition to the frequency of stimulation and number of motor units recruited, the strength of a muscle contraction can also be altered by changing the starting length of a muscle. This is called the (blank)

A

length-tension relationship

58
Q

How do you get the best contraction?

A

perfect overlap

59
Q

What happens if you overstretch?

A

you will have little overlap and a small force

60
Q

What happens if you have too little stretch?

A

you will be crowded and generate a weak force

61
Q

What is an isometric muscle contraction?

A

keep muscle the same length and generate a force

62
Q

What is an isotonic contraction?

A

constant force and apply tension, measure shortening and graph.

63
Q

What will the slope of an isotonic contraction give you?

A

velocity of shortening

64
Q

The heavier the load the (blank) the shortening velocity

A

smaller

65
Q

(blank) make up 10-15% of the protein in the body

A

myosins

66
Q

WHen you have a mutation in myosin you get a (blank)

A

muscle disorder

67
Q

What happens if you have a mutation in MyHC IIa (MYHC2)?

A

muscle myopathy

68
Q

What are the clinical features of muscle myopathy?

A

muscle weakness, atrophy near shoulders, back, hand and thigh musles.

69
Q

What is the pathogenesis of MyHC IIa (MYHC2)?

A

mutations primarily to SH1 helix in myosin, thought to alter actin-myosin ATPase activity

70
Q

What happens if you have a mutation to embryonic MyHC (MYH3)?

A

distal arthrogryposis. Freeman-Sheldon Syndrome, Sheldon-Hall syndrome

71
Q

What are the clinical features Freeman-sheldon syndrome etc.?

A

joint contractures with predominant distal involvement

72
Q

What is the pathogenesis of freeman-sheldon syndrome?

A

mutations in troponin I, troponin T, tropomyosin, perinatal myosin and embyronic myosin. thought to disrupt sarcomere development
(i.e regulatory proteins)

73
Q

What happens if you have a mutation in B-Cardiac myosin (MyHC7)?

A

Laing myopathy

74
Q

What are the clinical features of Laing myopathy?

A

weakness of ankle dorsiflexion and “hanging big toe”

75
Q

What is the pathogenesis of B-cardiac myosin?

A

mutation in LMM region of myosin. Thought to disrupt myosin filament formation or disrupt interactions with myosin binding proteins like titin

76
Q

What are 5 factors that affect muscles ability to generate force and to contract?

A 
myosin isoforms
frequency of stimulation
number of motor units stimulated
degree of stretch (frank-starling)
whether muscle is allowed to shorten (Force-velocity relationship)
77
Q

A complete muscle twitch is divided into what three phases?

A

latent, contraction, relaxation

78
Q

What is the latent period due to? So what does this mean?

A

AP, calcium

There is a delay between applied voltage and increase in tension

79
Q

What happens if you have a smaller time interval between contractions?

A

your second contraction will be bigger due to temporal summation of tensions

80
Q

What happens if you have continuous stimulation of a muscle?

A

temporal summation (as we apply more voltage, we get more stimulation, more release of calcium, stronger contraction), then we get tetanus (generating max force) and then fatigue (decreased tension)

81
Q

Asynchronous motor unit activity maintains a nearly (blank) in the total muscle

A

constant tension

82
Q

A motor neuron and all of the muscle cells it stimulated is called a (blank)

A

motor unit

83
Q

If we activate more than one motor neuron via an interneuron, what will our force be like?

A

increased due to recruitment

84
Q

The strength of a muscle contraction is determined not only by the frequency of stimulation but also by the (blank and blank) of motor units recruited

A

number and size

85
Q

In vivo, the number of motor units that are recruited is determined by the number of (blank) that are stimulated by the central nervous system

A

motor neurons

86
Q

In addition to the frequency of stimulation and number of motor units recruited, the strength of a muscle contraction can also be altered by changing the starting length of a muscle. This is called the (blank)

A

length-tension relationship

87
Q

How do you get the best contraction?

A

perfect overlap

88
Q

What happens if you overstretch?

A

you will have little overlap and a small force

89
Q

What happens if you have too little stretch?

A

you will be crowded and generate a weak force

90
Q

What is an isometric muscle contraction?

A

keep muscle the same length and generate a force

91
Q

What is an isotonic contraction?

A

constant force and apply tension, measure shortening and graph.

92
Q

What will the slope of an isotonic contraction give you?

A

velocity of shortening

93
Q

The heavier the load the (blank) the shortening velocity

A

smaller

94
Q

(blank) make up 10-15% of the protein in the body

A

myosins

95
Q

WHen you have a mutation in myosin you get a (blank)

A

muscle disorder

96
Q

What happens if you have a mutation in MyHC IIa (MYHC2)?

A

muscle myopathy

97
Q

What are the clinical features of muscle myopathy?

A

muscle weakness, atrophy near shoulders, back, hand and thigh musles.

98
Q

What is the pathogenesis of MyHC IIa (MYHC2)?

A

mutations primarily to SH1 helix in myosin, thought to alter actin-myosin ATPase activity

99
Q

What happens if you have a mutation to embryonic MyHC (MYH3)?

A

distal arthrogryposis. Freeman-Sheldon Syndrome, Sheldon-Hall syndrome

100
Q

What are the clinical features Freeman-sheldon syndrome etc.?

A

joint contractures with predominant distal involvement

101
Q

What is the pathogenesis of freeman-sheldon syndrome?

A

mutations in troponin I, troponin T, tropomyosin, perinatal myosin and embyronic myosin. thought to disrupt sarcomere development
(i.e regulatory proteins)

102
Q

What happens if you have a mutation in B-Cardiac myosin (MyHC7)?

A

Laing myopathy

103
Q

What are the clinical features of Laing myopathy?

A

weakness of ankle dorsiflexion and “hanging big toe”

104
Q

What is the pathogenesis of B-cardiac myosin?

A

mutation in LMM region of myosin. Thought to disrupt myosin filament formation or disrupt interactions with myosin binding proteins like titin

105
Q

Point mutations to B-cardiac myosin, actin, troponin, and tropomyosin have been linked to (blank) and (Blank)

A

FHC (familial hypertrophic cardiomyopathy)

DCM (dilated cardiomyopathy)

106
Q

Myosin mutations cause (blank) and sudden death

A

familial hypertrophic cardiomyopathy

107
Q

FHC mutations (blank) myosin force generation

A

enhance

108
Q

DCM mutation (blank) myosin force generation

A

decrease

Block 4 Week 1 Dani (10 decks)

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