Ctyoskeleton Flashcards

1
Q

actin assembly

A

1) formin initiates formation (rate limiting step)
2) G (globular) actin-ATP add together to make dimer, the trimers, then chain of F (filamentous) actin
3) keep adding G actin-ATP to plus(+) end = elongation
4) branching initiated by Arp2/3

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2
Q

treadmilling

A

actin can be in steady state- G actin-ATP are added to + end, at same rate G actin -ADP are removed from - end

plus end -> barbed end; minus end -> pointed end

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3
Q

regulatory proteins of actin filament

A

formin-initiates assembly of actin filaments and usually stays there
Arp2/3-starts branching
cofilin-clips and dissociates G actin monomers from F actin chain
profilin- replaces ADP w/ ATP on G actin
CapZ-binds + end to prevent degradation
tropomodulin-binds - end to prevent degradation

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4
Q

filamin

A

crosslinks actin as it forms networks (similar to collagen IV)

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5
Q

fimbrin

A

holds actin filaments close together in parallel in forming actin bundles

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6
Q

alpha-actinin

A

holds actin filaments farther apart than fimbrin in actin bundles

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7
Q

Actin in cell migration

A

when a cell migrates is sends a leading edge, attached, and then retracts/pulls the rest of the cell up with it
actin must move with and support the cell
filopodia-actin filament goes out to farthest extensions to lead
lamellipodia-actin bundles follow

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8
Q

filopodia movement of actin filament

A

“Leading”

in order for actin filament to move towards the edge of the cell membrane, cofilin must remove G actin-ADP from -end, then twinfilin attaches to the G actin monomer, then profilin attaches and kicks off twinfilin and replaces ADP w/ ATP, then G actin-ATP is taken to +end where WASP/Scar (activates Arp2/3) and barbed end tracking protein add to F actin

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9
Q

Wiskott Aldrich Syndrome

A

X-linked immune disorder that creates a defect in the WASP/Scar protein that allows F actin to from branches to make filopodia for cell movement
babies w/ wiskott aldrich bleed because their platelets/actin cytoskeleton don’t work right and they get a lot of infections because their immune system doesn’t work right

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10
Q

myosin

A

moves stuff across the cell by binding a vesicle and then using actin filaments as a railroad system across the cell

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11
Q

3 cytoskeletal proteins

A

1) actin
2) intermediate filaments
3) microtubules
inc in size

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12
Q

intermediate filaments

A

medium sized cytoskeletal protein
cell specific, differ by cell
can assemble at both ends

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13
Q

assembly of IF

A

1) 2 polypeptides twist into a dimer

2) 2 dimers stack to form a tetramer, do not twist

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14
Q

microtubules

A

largest cytoskeletal protein
13 protofilaments of alpha-tubulin and beta-tubulin formed around a hollow center cylinder
inherently unstable
cell shape, cell locomotion, transport w/in a cell, important in cell division (pulls apart chromatid)

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15
Q

microtubule polymerization

A

originate from a centrosome
alpha-tubulin and beta-tubulin leave from the -end
and are added to the +end

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16
Q

dynamic instability of microtubules

A

in a cell, a cap tends to cover the -end of microtubules, preventing them from leaving there
the microtubules rapidly grows and shrinks from the +end depending on the amount/rate of phosphorylation of tubulin monomers

growth->more alpha or beta tubulin-ATP is being added than what is being hydrolyzed to tubulin-ADP
shrinkage/catastrophe->hydrolysis of ATP to ADP happens faster than alpha or beta tubulin-ATP is added

CLASP stops disassembly and rescues the microtubule by restarting assembly (ADP->ATP)

17
Q

organization of microtubules in nerve cell

A

In axon: +end always away from cell body, and -end always towards cell body
In dendrite: + and - ends can go both ways

there are binding proteins attached to the microtubules for stabilization:
On microtubules in axon->tau
On microtubules in dendrite->MAP2

MAP2 also acts to connect microtubules to IFs

in Alzheimer’s tau is not properly degraded and clumps

18
Q

kinesin

A

microtubule motor protein that carries vesicles away from - end (centrosome side) to + end
requires ATP

19
Q

dynein

A

microtubule motor protein the carries vesicles from + end to - end
requires ATP

20
Q

cilium axoneme

A

most prominent structural component of cilium (also flagellum)
9:2–> 9 microtubule doublets around a ring for movement, and an additional pair of fully formed microtubules in the center for stability and support
9 pairs are made of an A tubule that is fully former, and a B tubule that is not fully formed and attached to the A tubule
nexin-protein that makes sure A and B tubules stay together
basal body-where cilia grow from, are anchored from (9-2 start here)
9 pairs of microtubules make the cilia/flagella move by dynein walking towards the basal body, as one “foot” is one the A tubule of one doublet and the other foot is on the B tubule of the adjacent doublet

smoking clogs cilia in respiratory passages