Cell Bio Exam 3

plus end

barbed end of actin filament

minus end

pointed end of actin filament

Thymosin B4

actin sequestering protein, binds monomers and prevents polymerizing

Profilin

promotes G actin to exchange ADP for ATP, binds to + end and promotes polymerization on existing filaments

cofilin

severs ADP actin filaments causing minus end depolymerization, creates new plus end for growth

formin

actin nucleator that generates long unbranched filaments, dimerizes, facilitates plus end growth, remains attached to plus endof actin filaments during polymerization.

tandem actin monomer-binding proteins

actin nucleator that creates unbranched filaments, remains at the minus end

Arp 2/3 complex

actin nucleator that generates branched filaments, 7 subunits, caps new filament at minus end

WASP

family of proteins that helps Arp 2/3 nucleate filaments, activated by small GTPases (Cdc42-GTP) to assemble actin in membrane protrusions

phalloidin

prevents actin filament depolymerization, binds at the interface between subunits

cytochalasin

prevents elongation of actin, binds to plus ends and caps them, filaments eventually depolymerize, reversible

latrunculin

prevents actin monomers polymerizing into filaments (sequesters them), rapid disassembly of filaments, reversible

taxol

binds to MTs and stabilizes, prevents disassembly, prevents cancer cells from dividing

cholchicine

binds to tubulin dimers and when they’re polymerized prevents further polymerization, creates a GDP cap, reversible

nocodazole

binds to tubulin subunits and triggers depolymerization, reversible

yTURC

anchors the MTS at the MTOC

Cap2

stabilizes actin filaments by binding to plus end

tropomodulin

stabilizes actin filaments by capping minus end

tropomyosin

stabilizes actin filaments by binding along their length

gelsolin

severs actin filaments and remains bound to plus end, activated by increased calcium

filamin and septin

actin cross-linking proteins, long and flexible spacer domains, create gel-like networks

fimbrin

actin cross-linker with short, rigid spacers, creates aligned bundles, similar to vilin and fascin

a actinin

actin crosslinker that links filaments into bundles arranged into parallel and antiparallel arrays, involved with contraction, forms a head to tail dimer that motor proteins can fit through

ezrin (ERM protein)

linker between actin and integral membrane proteins

spectrin

connects actin to membrane proteins, creates skeleton adjacent to plasma membrane

dystrophin

links cortical actin to muscle cell membranes via Dystroglycan complex

hereditary spherocytic anemias

mutations in RBC actin membrane skelton

Duchenne muscular dystrophy

mutation in dystrophin creates weakened muscle cell plasma membranes

stathmin

binds and sequesters tubulin oligomers, promotes catastrophe and depolymerization

+TIPs

bind to the plus ends of microtubules

EBI

+TIP, regulates end dynamics and link MTs to organelles

CHIP-170

+TIP, mediates plus end interactions with membranes and chromosomes

katanin

severs MTs and promotes depolymerization at minus ends

Kin13

promotes depolymerization at the plus end of MTs by binding to and inducing protofilament curling

MAPs

stabilize plus ends of MTs and accelerates assembly

MAP2

organizes MTs in neuronal axons and dendrites, longer projection domain with greater spacing

Tau

organizes MTs in neuronal axons and dendrites, shorter projection domain, aggregation is associated with Alzheimers

myosin I

short tails, single-headed, tails with actin binding site can mediated movement of filaments past eachother, or tails with membrane binding binding sites attach to vesicles/organelles

myosin II

dimer, creates myosin thick filaments, long alpha helical tails mediate dimerization and further polymerization

myosin V

dimer, organelle transport, walk along F-actin, processive movement, 72 nm setp

myosin VI

only - end directed myosin

Kin N Kinesins

MT associated motor protein class, plus end directed, motor domain at N-terminus, Kin 1, 2, 5

Kin C Kinesins

MT associated motor protein class, C-terminal motor domain, moves towards - ends

Kin I Kinesins

MT associated motor protein class, internal motor domain, promote protofilament peeling

Kin 1

conventional kinesin, 2 heavy chains: motor domain at N terminus, alpha helical coiled tails; 2 light chains: at ends of tails, mediate interactions with membrane vesicles

Kin 5

bipolar, Kin N, moves 2 antiparallel MTs in opposite directions, stabilize polar MTs and prevent catastrophe

lamellipodia

leading edge of moving interphase cell, thin sheet-like structures, branched network of actin

filopodia

thin needle-like projections on leading edge, tight parallel actin bundles

stress fibers

long anti parallel cables of actin, function in cell adhesion and control, along lower surface of cell, ends terminate at integrin-containing focal adhesions

Myosin Light Chain Kinase (MLCK)

phosphorylates myosin II light chains to contract stress fibers

Cdc42

activates WASPs and Formins > actin polymerization > filopodia formation

Rac

activates WAVE > activates Arp 2/3 > actin polymerization > lamellipodia formation

Rho

activates Rho Kinase > myosin activity > stress fiber contraction

activates Formin > actin polymerization > stress fiber formation

condensins

ATPases, work with topoisomerases to drive DNA supercoiling and compacting

cohesions

proteins that hold sister chromatids together at the centromere

aster

radial array of MTs nucleated by duplicated centrosomes that move them to opposite sides of the nucleus

kinetochore MTs

attach the kinetochore of chromosomes to the spindle poles

polar MTs

radiate from one pole and attach to antiparallel MTs emanating from the opposite poles by Kin-N kinesins

astral MTs

face away from the central spindle and mediate the interaction of the spindle with the cell cortex

Kin 14

Kin C, opposes force of Kin 5 in overlap zone, prevents overelongation

congression

overall movement of captured chromosomes toward the equator of the spindle, bi-directional movement of bi-oriented chromosomes near the equator

poleward MT flux

minus ends being depolymerized by Kin 13 causes treadmilling effect, pushes chromosome to pole depending on which end is growing faster

poleward ejection force

chromokinesins move chromosomes towards the plus ends of polar MTs at spindle equator

chromokinesins

Kin N, located on chromosome arms

Anaphase A

kinetochore MTs shorten and chromosomes move toward poles (MT depolymerization at both + and - ends)

Anaphase B

polar MTs elongate and poles move farther apart (dyneins at cell membrane and kinesins at overlap zone)

Anaphase promoting complex

activated by Cdc 20, polyubiquinates securin which releases separase

separase

enzyme that degrades cohesins connecting sister chromatids

CENP-E

Kin N, keeps chromosomes associated with plus ends of MTs, at kinetochore and Ndc80 complex

RhoA

Rho GTPase that marks the cleavage site and causes nodes to accumulate formin and myosin II

midbody

ring of membrane flanked on both sides by MT bundles, where membranes eventually split during cytokinesis