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Cell Biology of Disease > Cytoskeleton > Flashcards

Cytoskeleton Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What are actin filaments made from?

A

Actin polymer

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2
Q

What are microtubules made of?

A

Alpha-beta tubulin dimers

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3
Q

What are intermediate filaments made from?

A

Intermediate filament proteins

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4
Q

What acin polymerises into F-actin?

A

G-actin

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5
Q

How many other subunits does F-actin contact ?

A

Three, along the strand and between the two strands

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6
Q

Structure of mysoin

A
  • Myosin (class 2) is a hexameric protein:
  • Two heavy chains dimerise (via the coiled coil) to form the coiled-coil tail
    and two globular myosin heads
  • Each myosin head is composed of a motor domain and a lever.
  • The lever contains 2 ‘IQ’ motifs (IQxxxRGxxR)
  • Light chains bind to the IQ motifs – two per lever (two per heavy chain)
  • Essential light chain (ELC) binds to an IQ motif close to the motor
  • Regulatory light chain (RLC) binds to the IQ motif close to the coiled coil
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7
Q

Hypertrophic cardiomyopathy (HCM)

A

Autosomal dominant, typical missense mutations in genes encoding sarcomeric proteins. Left ventricular hypertrophy and myofibrillar disarray

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8
Q

Mutations in MYH7 cause what disease?

A

HCM

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9
Q

Mutations in MYBPC cause what disease?

A

HCM

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10
Q

Mutations in loop 1, converter and relay helix likely affect what?

A

Force generation

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11
Q

Mutations in S2 affect

A

Interacting heads motif, more ATP usage. Could affect binding of MyBPC

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12
Q

Mutations in non muscle myosin 2A cause these diseases

A

Blood clotting disorders, deafness and kidney disorder

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13
Q

What does the activation of platelets depends on?

A

NM2A and actin

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14
Q

What do smooth and non-muscle myosin 2 isoforms form?

A

10S shutdown state.

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15
Q

What are smooth and noon-muscle myosins activated by?

A

Phosphorylation of the RLC

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16
Q

Mutations in MYH9 cause what disorders?

A

Bleeding

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17
Q

Mutations in skeletal muscle actins can cause

A

Skeletal muscle myopathies

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18
Q

What mutations cause Baraitser-Winter syndrome?

A

Mutations in beta and gamma actins

19
Q

Symptoms of Baraitser-Winter syndrome

A

Changes around the eyes: (congenital ptosis
(drooping eyelid),
* High-arched eyebrows,
* Hypertelorism (increased eye spacing),
* Missing tissue around the eye (Ocular colobomata)
* Brain malformation - anterior predominant
lissencephaly.
* May also be short
* May also have microcephaly, intellectual disability, seizures and hearing loss

20
Q

What is critical to forming a highly folded brain?

A

Neuronal migration

21
Q

What is important for neuronal migration?

A

Non muscle actins

22
Q

Keratin is an example of what type of fibre?

A

Intermediate

23
Q

What filaments are required for cell to cell and cell-ECM adhesion?

A

Intermediate

24
Q

What happens in the skin epidermis basal layer?

A

Cells adhere to underlying extracellular
matrix through focal adhesions
(hemidesmosomes)
Cells divide (proliferate) - express K5
and K14
Then migrate upwards to spinous layer:
Switch keratin isoform expression to K1
and K10

25
Q

Mutations in keratin 5 and 14 cause

A

Epidermolysis bullosa

26
Q

mutations in Keratin 1 and 10 cause

A

Epidermolytic Hyperkeratosis

27
Q

What is found at the fast growing end of microtubule tubes?

A

Beta-tubulin which hydrolyses GTP, can exchange GDP for GTP.

28
Q

Do both alpha and beta tubulin bind GTP?

A

Yes

29
Q

Does beta tubulin hydrolyse GTP?

A

Yes, only.

30
Q

What part of microtubules can be PTM’ed?

A

C terminal tails

31
Q

What are microtubules essential for?

A

Cell migration, cargo transport, mitosis and formation of synapses and neuronal cells.

32
Q

What are the two types of motor proteins?

A

Kinesin and dynein

33
Q

How many types of kinesin are there?

A

Many, about 40, some specialised for trafficking like Kif5 (kinesin-1).

34
Q

How many types of dynein?

A

One, cytoplasmic.

35
Q

Which end does kinesin-1 move on microtubules?

A

Plus end

36
Q

Which end of microtubules does dynein move to?

A

Minus

37
Q

Description of TUBA1A mutation derived disease

A

Cause microcephaly, developmental delay, epilepsy, lissencephaly (smooth brain).

38
Q

What residue is commonly mutated in TUBA1A

A

R402

39
Q

What cell type are microtubules critical for?

A

Neurones

40
Q

What is KIF1A for?

A

Anterograde transport, veiscles for pre and post synaptic assmebly. Autophagy

41
Q

What is KIF1C for?

A

Anterograde cargo transport and retrograde transport between Golgi and ER

42
Q

What disease can Kif5A mutations cause?

A

Hereditary spastic paraplegia (SPG10), amytrophic lateral scleosis (ALS), Charcot-Tooth-Marie tyoe 2 (CMT2)

42
Q

Exon 27 deletion leads to what?

A

Aggregation

Cell Biology of Disease (9 decks)

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