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Health and Disease Semester 1 > Cytoskeleton > Flashcards

Cytoskeleton Flashcards

1
Q

What is the cytoskeleton sold in mitosis?

A

During anaphase to pull the chromosomes apart and to split the dividing cell into two.

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2
Q

What are the three types of filaments in the cytoskeleton?

A

Actin, microtubules and intermediate filaments.

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3
Q

What is actin for?

A

To determine the shape of the cells surface as it lies under the plasma membrane and it’s necessary for whole-cell locomotion.

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4
Q

Describe actin?

A

5-9 nm diameter, 375 amino acids and 42 kD double-stranded helical polymers of the protein actin in bundles

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5
Q

How many types of actin are there?

A

Three, alpha (muscle), beta and gamma (both non-muscle).

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6
Q

What are the plus and minus ends of actin?

A

Plus end is the fast growing end and the minus end, aka the barbed end, is the slow growing end.

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7
Q

What disease are associated with actin?

A

Congenital myopathies, duchene muscular dystrophy, blood disorders

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8
Q

What’s the most common congenital myopathy?

A

Nemaline

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9
Q

What symptoms do congenital myopathies have?

A

Weak muscles due to lack of sarcomeres, floppy and may require support breathing (ventilation), feeding, standing, sitting etc. Facial weakness and scoliosis are also common.

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10
Q

Do congenital myopathies get worse with age?

A

No.

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11
Q

What are the different types of congenital myopathies?

A

Nemaline, actin, intranuclear rod and nemaline with core like areas.

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12
Q

What is duchene muscular dystrophy caused by?

A

Mutations in dystrophin.

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13
Q

Why does duchene muscular dystrophy mostly effect boys?

A

As the gene is on an X chromosome, 100 Boyes per year.

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14
Q

What is dystrophin?

A

A protein found close to the plasma membrane in skeletal and cardiac muscle which links internal cytoskeleton to extracellularly matrix.

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15
Q

What are the symptoms of duchene muscular dystrophy?

A

Muscle weakness and necrosis.

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16
Q

Does duchene muscular dystrophy get worse with age?

A

Yes

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17
Q

Name a blood disorder from mutations in non-muscular myosin?

A

Griscelli syndrome and usher syndrome

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18
Q

What are some symptoms of blood disorders due to actin?

A

Deafness and blindness in usher syndrome.

19
Q

What does the cytoskeleton allow?

A

Organisation in space, correct shape, robust and proper structure and the ability to rearrange the internal components and mechanical interaction with the environment.

20
Q

What do microtubules do?

A

Determine the positions of membrane-enclosed organelles and direct intracellular transport.

21
Q

Describe microtubules?

A

25 nm long, rigid, straight, hollow cylinders made of the protein alpha-beta dimer tubulin

22
Q

What is one end of the microtubule usually attached to?

A

Centrosome: MTOC- microtubule organising centre

23
Q

Why could microtubules be a good target for cancer?

A

As they are required for the rapid division of cells. Taxol has been used as a cancer treatment.

24
Q

What can microtubules form?

A

The core of the flagella and cilia.

25
Q

Why could microtubules be described as tentacles?

A

As they are dynamic and grown and shrink to explore the cytoplasm.

26
Q

What two MAPs are microtubules tracks for?

A

Kinesin and dynein.

27
Q

How are kinesin and dynein different?

A

Kinesin takes 8nm steps, powered by ATP towards the plus end whereas dynein goes towards the minus end.

28
Q

What can bind to stabilise/destabilise microtubules?

A

Other MAPs, eg. Tau binds to the end and MAP2 binds to the cell body.

29
Q

What disease are found in microtubules/kinesin/MAPs?

A

Tauopathies, lissencephaly, hereditary specific paraplegia.

30
Q

Name some tauopathies?

A

Alzheimer’s, progressive supra nuclear palsy, corticol-basal degeneration, dementia, Parkinson’s etc.

31
Q

What does tau do in tauopathies?

A

Binds and stabilises microtubules normally but when hyper phosphorylated due to the down regulation of protein phosphatase 2A it is released. This causes the microtubules to dissemble, and the tau can for, paired helical filaments and neurofibrial tangles which compromise axonal transport.

32
Q

What is lissencephaly?

A

Absence of normal folds in the brain caused by a tubulin mutation.

33
Q

What are the symptoms of lissencephaly?

A

Abnormally small head, unusual facial appearance, difficulty swallowing, failure to thrive, muscle spasms, seizures and severe psychomotor retardation, usually death before 2 years of age.

34
Q

Describe the mutation that causes lissencephaly?

A

Tubulin mutation results in missfolding of the tubulin effecting dimerisation and binding to other microtubule proteins. First mutation to be found was a missense Arg264 to Cys264 and since many others have been found.

35
Q

What mutation causes hereditary specific paraplegia?

A

Missense mutation in motor domain of kinesin-1, effecting movement and binding of cargo.

36
Q

What are the symptoms of hereditary specific paraplegia?

A

Progressive weakness, stiffness in legs all due to synapses not being used and therefore wasting away. Can be late onset (24 years etc) and is very rare.

37
Q

What do intermediate filaments do?

A

Provide mechanical strength. One type forms a mesh-like nuclear lamina lining the inner face of the nuclear envelope, which is a protective cage for the cell’s DNA. Important for cell-to-cell and cell-to-ECM adhesion.

38
Q

Describe intermediate filaments?

A

10 nm diameter, rope-like fibres which twist into sting cables.

39
Q

What disease can occur due to intermediate filaments?

A

Keratin mutations: epidermolysis bullosa
Desmin mutations: desminopathies
Nuclear lamina mutations

40
Q

What are the symptoms of epidermolysis bullosa?

A

Blistering of the skin due to lack of cell-to-cell adhesion.

41
Q

What do desminopathies effect?

A

Skeletal, cardiac and smooth muscles.

42
Q

What can lamin A mutations cause?

A

Progeria, emery dreiffus muscular dystrophy, limb girdle muscular dystrophy, dilate cardiomyopathy and charcot-marie-tooth disease.

43
Q

What are accessory pigments?

A

Proteins that are vital for lining the filaments to other cell components as well as to each other and the controlled assembly of the cytoskeletal filaments to articulate locations.

Health and Disease Semester 1 (14 decks)

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