Actin/Cytoplasmic Filaments and Cell Motility Flashcards

1
Q

Microtubule functions

A

Transport

Organelle arrangement

Mitosis

Cilia & flagellar movement

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2
Q

Microfilament functions

A

Muscle contraction

Cell adhesion & motility

Microvilli

Smallest but most common

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3
Q

Functions of intermediate filaments

A

Mechanical integrity

Motility

Scaffolds

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4
Q

Duchenne Muscular Dystrophy

A
  • X-linked mutation –> complete absence of dystrophin –> plasma membrane of muscle cells tears during contraction
  • Progressive
  • Walking on toes; protruding abdomen; shoulder & arms held back; weakness and muscle wasting
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5
Q

Dystrophin

A

Links actin to the extracellular matrix by bindin a,B dystroglycan on the plasma membrane, which binds laminin*, perlecan, and agrin in the ECM

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6
Q

Becker’s muscular dystrophy

A

Lower expression levels of dystrophin; less severe w/later age of onset than DMD

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7
Q

Why do people with DMD have enlarged calves?

A

Damaged muscle tissue –> fibroblasts migrate there to replace destroyed muscle with collagen and scar tissue

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8
Q

How does ATP control the formation of actin filaments?

A

ATP-G-actin is added more quickly to the + end, and polymerization activates the intrinsic ATPase activity of actin –> hydrolysis and dissociation of ADP+Pi makes the actin less stable such that it falls off at the - end

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9
Q

What binds to ATP-G-actin and sequesters it from polymerization?

A

Thymosin B4 and profilin

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10
Q

The (+) end of F-actin as a ___er critical concentration for ATP-G-actin, which is why it’s added more efficiently at the (+) end

A

lower critical concentration

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11
Q

Cofilin

A

Binds F-actin subunits with ADP and breaks it into shorter pieces –> more (-) ends for disassembly

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12
Q

Profilin

A

Enhances exchange of ADP for ATP on free G-actins –> regenerates more ATP-G-actin but also sequesters it

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13
Q

Thymosin B4

A

Binds ATP-G-actin to sequester it form polymerization until there’s too little

Maintains a steady state level of F-actin

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14
Q

Tropomodulin

A

Binds at the (-) end to stabilize F actin

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15
Q

CapZ

A

Binds at the (+) end to prevent further polymerization

Controlled by signal transduction molecules and other regulatory proteins

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16
Q

Formin

A

Proteins that stimulate assembly of long, linear F-actin in stress fibers and contractile rings

17
Q

Fibrim

A

organizes filaments into microvilli

18
Q

Arp 2/3 & WASp

A

Stimulates formation of branched filaments in the leading edge of cells

Controlled by signal transduction processes

19
Q

Function of spectrin

A

Organizes microfilaments at the cell cortex

20
Q

How do CDC42 and WASP control actin assembly?

A

CDC42 is a small GTPase of the Rho family activated by growth factors; it activates WASp to nucleate actin filaments by Arp2/3 complex

21
Q

During cell migration, what 4 things are happening?

A
  • Leading edge:
    • Extension of plasma membrane to form lamellipodium by increasing length of actin
    • Adhesion of lamellipodium
  • Translocation: bulk of cell cytoplasm moves forward
  • Back of cell: De-adhesion & endocytic recycling of adhesion points as stress fibers contract
22
Q

In the leading edge of a mgirating cell, extension is nucleated by ___ and controlled by __ and __, two signaling GTP-binding proteins activated by growth factor cascade

A

Nucleated by Arp2/3

Controlled by Cdc42 and Rac

23
Q

At the trailing edge, ___ is a GTP-binding protein that signals activation of formation and..

A

Rho

  • Activates rho kinase, which activates myosin II to contract the back of the cell
  • Blocks Rac
24
Q

a-actinin

A

Organizes the F-actin of the stress fibers during migration; also important in muscle contraction

25
Q

Integrins

A

Transmembrane proteins that bind to the cytoskeleton and the ECM to fix cells into their tissues, forming focal adhesions

A nonmotile cell expresses integrins to keep it in place; also used to generate intercellular signals that lead to focal adhesions

26
Q

Lamellipodia vs Filopodia

A

Lamellipodium: projection of polymerized actin mesh on leading edge; whole structure propels the cell across a substrate

Filopodia: ribs of actin within lamellipodia that spread beyond the lamellipodium frontier

27
Q

Hereditary sphereocytosis

A

RBCs are small and fragile because of a defect in spectrin, protein 4.1, or ankyrin –> lack of cortical connections with plasma membrane –> anemia, hepatomegaly, bilirubing allstones

28
Q

Epidermolysis bullosa

A

Mutations of keratins 5 or 14 causes defects in the junction between dermis & epidermis

29
Q

Intermediate filaments are not dynamic and don’t require ATP for polymeriazation; instead __ controls subunit exchange

A

Phosphorylatoin

30
Q

ALS/Lou Gehrig’s disease

A
  • Mutations affecting various neurofilaments –> abnormal accumulations of neurofilaments (spheroids or Lewy body-like deposits) in motor neurons
  • 10% of ALS cases are familial (FALS), typically AD
  • 8 different mutations in the profilin1 gene (PFN1) are associated with FALS
31
Q

You can characterize cancers via IF’s.

A metastic tumor stians positive for acidic and basic keratins. From what cell type did this tumor most likely originate?

A

Epithelium

32
Q

Neurons have what type of IF’s?

A

neurofilaments and lamins

33
Q

Muscle cells, glial cells, and mesenchymal cells have what IF’s?

A

Desmin

Vimentin

GFAP

34
Q

What’s the problem?

A

Duchenne Muscular Dystrophy

Scar tissue (collagen+blood vessels) repalcing the muscle fibers –> contraction of fibrous scar tissue around muscle cells causes muscle deformity and dysfunction

35
Q
A