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lecture 10 Flashcards

1
Q

what happens when cell migration goes wrong

A

metastatic cancer

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2
Q

how do cells move?

A

mesenchymal cell migration, amoeboid cell migration

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3
Q

what are both migrations driven by

A

lamellipodial protrusions at leading edge

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4
Q

what is diff b/w ameboid and mesenchymal

A

ameboid is less adhesive

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5
Q

how do cells bind to extracellular env.

A

integrin receptors / extracellular matrix

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6
Q

descibe mesenchymal migration

A

fibroblasts; adhesion, harder to move, stuck to environment

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7
Q

describe ameboid migration

A

immune cells; move quicker, slip through to chase down pathogens

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8
Q

2 main ways for cells to move

A

lamellipodia (high or low adhesion), blebbing migration

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9
Q

step 1 of cell moving

A

adhere to surface (integrin receptors)

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10
Q

step 2 of cell moving

A

flatten and spread (integrin, actomyosin)

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11
Q

step 3 of cell moving

A

become polarized (tell front from back; microtubules)

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12
Q

step 4 of cell moving

A

generate protrusions (actin filaments; facilitates polarization)

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13
Q

step 5 of cell moving

A

form new adhesions, release old ones (combo of all 3)

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14
Q

step 6 of cell moving

A

directionally migrate intracellular signaling

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15
Q

how are epithelial cells that line surface anchored to underlying matrix

A

integrin adhesions

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16
Q

what happens if you disrupt integrin adhesions

A

would wipe cells right off dermis

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17
Q

what is cell matrix adhesion mediated by

A

integrin receptors

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18
Q

what happens when u see fiber laying across cell

A

it’s bound by integrins entire length of filament

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19
Q

what are integrins

A

transmembrane heterodimers that link ECM to cytoskeleton

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20
Q

what is collagen

A

glue that holds tissue and organs together

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21
Q

what binds to collagen fiber

A

integrin receptors

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22
Q

on cytoplasmic face, what connects to adhesions

A

actomyosin filaments

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23
Q

what does this mean for contractility

A

as actomyosin force is applied, attached to integrin, so pulling force is gonna be applied to outside env. (ECM)

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24
Q

what does alpha subunit do

A

participates in adhesion; facilitates adheion strength

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25
what does beta subunit do
connects complex to actin filaments inside cell
26
vinculin
force sensor that triggers signaling
27
what does actin bind to
vinculin, talin (connects everything to integrin)
28
what does this machinery represent
continuous mechanical connection from ECM (outside) to cytoskeleton (inside)
29
describe integrin activation
can be off or on
30
describe integrin at surface
active
31
what happens once integrin active
at cell surface, binds to matrix and talin
32
what happens through talin
binds to vinculin (adaptor protein that links integrin complex to actin filaments)
33
what happens when you get force/contractility
positive feedback loop, more integrins, more actomyosin filaments, bigger+stronger adhesions, more effective force
34
does this positive feedback loop happen in fibroblasts or immune cells
fibroblasts
35
what happens when integrin binds to talin
talin recriuts vinculin
36
how is force sensed by adhesion complexes
talin
37
what is talin
mechanosenser responsible for detecting pulling force on connecitions
38
what happens when it detects force
trigger that regruits more actomyosin contractility in positive fedback loop, to ramp up contractility to allow adhesions to grow and strengthenh
39
how does protein sense force
force causes change in confomration of protein, revealing a hidden binding site
40
what happens when they pull on talin
talin unfolds (force dependent conformational chaneg)w
41
what happens when talin unfolds
reveals binding site for vinculin
42
what happens when vinculin is binded
joins talin; more actomyosin filaments come w/ vinculin --> positive feedback loop controlled by talin
43
where does integrin recruit intracellular signaling proteins
sites of cell-matrix adhesion
44
what gives increased contractility that helps in adhesion formation
rhoA activaetes ROCK, phosphorylates myosn light chain , activates myosin 2 protein
45
what's happening at bottom/back of cell
adhesions falling apart, disassembed, recycled into cytoplasmw
46
what wud happen if cell douln't dissasmeble adhesions in the back
cell would get stuck;
47
what does myosin contraction and cell adhesoin allow
allows cell to pull itself forward
48
what happens if nothing to anchor the netowrk
not gonna be able to push network forward, rather it pushes it back (cuz it's not yet attached to actomyosin machinery)
49
what happens when pos feedback loop
vinculin & talin grab actin filaments, harness contractile power to anchor filaments, now it can actually push it forward
50
retrograde flow
if filaments aren't anchored, netowrk is pushed backward
51
what happens if filaments aren't anchored
network pushed backward
52
what happens if filaments anchored
resist backward pushing force, exert force to make cell migration
53
what happens if cell bound to integrin
migrates; does work
54
what happens when new adheson forms
small, low contractility; need massive increase in contractility (vinculin, talin)
55
what needs to happen for recycling
not bound to talin; detach from it
56
what happens if rhoA is inhibited
contractility drops, breaks positive feedback loop, everything falls apart
57
what happens if vinculin mutated
you'd never get positive feedback loop initiated in first place
58
what happens if talin mutated
binding site always exposed; positive feedback all the time
59
role of myosin
help unfold talin, and strengthen adhesions through additional vinculin binding
60
what happens when integrins bind to ECM
talin unfolded, positive feedback loop for actomyosin contractility
61
what is any movement in ECM from
contractile forces in cell
62
what gives cell ability to propel itself forward
force is being transmitted from actomyosin filaments in cytoplasm, connected to alpha beta integrins via vinculin-talin, those integrins are connected to extracellular matrix
63
describe actin-integrin
continuous mechanical connection that allows cellular forces to pull on those extracellular fibers to allow for productive cell migration
64
2 major outcomes of force coupling
protrusion, traction forces against extracellular env.
65
what motor protein delivers cargo at MT tracks
kinesin 1; takes vesicles at golgi to plus ends
66
describe mesencyhmal cell migration
rac1 activates arp2/3, leads to actin polymerization, causes lamellipodial protrusion
67
what happens if RAC1 arp2/3 pathway is active W/O coupled at adhesions
no protrusion, just retrograde flow
68
what happene whenever rac1 activated
lamellipodia is formed
69
is contractility at leading or lagging edge
leading edge; adhesions
70
describe contractility at back of cell
RhoA, contractile forces that allow leading edge to contract and keep up w/ front
71
what contracts in the back?
actomyosin filaments that are attached to plasma membrane, as they are acted on by mosin 2 they become more tightly cross-linked, the spaces shrink, just continuously pulls plasma membrane forward
72
what is front rhoA contractility
plugs talin via vinculin to strengthen adhesions
73
what is back rhoA stuff
no adhesions; just contracting the actomyosin network underneath plasma membrane to contract the rear and allow it to move in synch w/ front of cell
74
what allows for continuous lamellipodia and cell migration
cofilin, at back of lamellipodial network (still front of cell), recycles monomers
75
describe how back of cell pulls itself forward
rhoA --> ROCK --> myosin 2
76
how does back of cell keep up w/ front
contraction in back
77
what does rhoA control
actomyosin contraction
78
what does rac1 control
lamellipodia (arp 2/3)
79
what does high contractility mean
low lamellipodia formation
80
what separates front from back of cell
cross talk b/w rac and rho
81
what do we need at front of cell fo r adhesion formation
rhoA
82
what does Rac1 do
activates arp2/3 for branched actin networks, turns on Pak, turns off actomyosin stressfibers
83
what does rac1 do to rhoA in front
suppresses rhoA response
84
describe cross-talk
chemoattractant binds GPCRs --> activate rac1 --> turn off rhoA
85
what happens as you get farther from cell
rac1 suppresses rhoA less and less; rhoA does actomyosin contractility more at the back
86
what is blebs
increase pressure to cause protrusion (no actin polymreization)
87
do blebs have actin
nah; just pressure driven

bio 211 (18 decks)

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