L8-9: Cell migration Flashcards

1
Q

What are the five steps of cell migration

A
  1. cell polarization
  2. leading edge protrusion
  3. leading edge adhesion
  4. cell body translocation
  5. trailing edge de-adhesion and retraction
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2
Q

How dose Rac1, Cdc42, Rho amount depend on the leading and trailing edge of the cell? How does this effect actin polymerization and contractility?

A

More Rac and Cdc42 in the leading edge > more actin polymerization. Less Rho > less contractility

Less Rac and CDC42 in trailing edge > less poly. More rho > more contractility

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3
Q

what sort of technique can be used to check Rac1 activation in cell?

A

optogenetics

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4
Q

What is the lamellipodia formation pathway?

A

Rac1 > wasp family > ARP > lamellipodia

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5
Q

What are the fastest cells in the world?

A

fish keratenocyte

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6
Q

In the leading edge, would cofilin be abundant near the edge of the cell? Why or why not? What is the function of cofilin?

A

it would be inside the cell. Cofilin is reponsible for actin depolymerization

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7
Q

Which complex helps with actin polymerization?

A

ARP complex

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8
Q

What are two essential proteins in trailing edge contractility?

A

Rho and Myosin II

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9
Q

Trailing edge contractility pathway?

A

Rho > Myosin II > parallel actin depoly

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10
Q

What is essential for actin and ECM connection? What is the process called?

A

Integrins. Focal adhesion

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11
Q

What does integrin bind to in cellular and extracellular side?

A

cellular: talin/paxilin + actin
extracellular: fibronectin

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12
Q

Explain molecular clutch hypothesis and its effect on protrusion during engaged clutch.

A

integrin binds to core proteins that act as friction to slow down actin treadmilling.

  • causes slower actin retrograde flow
  • stronger protrusion
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13
Q

Does the size of focal adhesion complex change cell migration speed? How?

A

too small > very little adhesion > slow ms
too big > too much adhesion > slow ms
only operates properly in the right size

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14
Q

What downstream proteins are effected by integrin based adhesion?

A

MAPK and ERK2. normal growth factor response is also increased.

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15
Q

Does the distribution of fibronectin matter in normal growth factor response? Why or why not?

A

well distributed fibronectin is needed. A single dense source of fibronectin doesnt allow cell movement and growth, resulting in cell apoptosis.

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16
Q

Integrin has its own kinase domain. True or False?

A

False

17
Q

Can src normally bind to FAK? Why or why not

A

FAK has an autoinhibitory loop that doesnt allow src binding.

18
Q

What allows src to bind to FAK?

A

integrin or growth factor activation

19
Q

Two downstream effects of src-FAK complex formation

A

Rho GAP and GEF

20
Q

Where does src bind FAK?

A

Tyr397