Cytoskeleton Part I (24) Flashcards by M B

what are the 3 types of cytoskeleton fibers?

microtubules

intermediate filaments

microfilaments

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microtubules

hollow & rigid cylindrical tubes

made of tubulin

responsible for movement from the interior to the exterior & vice versa, but not to the periphery

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which fiber is the largest of the cytoskeleton components?

microtubules

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What fiber offers the greatest amount of strength & durability?

microtubules

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microfilaments

solid, thinner structures

made of actin

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intermediate filaments

tough, ropelike fibers

made of a variety of related PROs

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Dynamic scaffold function of the cytoskeleton

Helps maintain cell shape

Shape is assoc with function

Resist mechanical restresses

Cytoskeleton can rearrange itself to change the shape of the cells

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Intracellular transport of the cytoskeleton

moves materials & organelles within the cell
mRNA
ER –> Golgi
Neurotransmitter containing vesicles
Peroxisomes (move to mitochondria to deal with free radicals)

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Force generation & motility of the cytoskeleton

move cells
Single-celled use cilia & flagella
Multicell use independent locomotion of an indiv cell
Dendrites stretch to make contact with the cell they need to make contact with & retract when necessary

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what type of cells are capable of independent locomotion?

sperm

white blood cells

fibroblasts

highly motile tip of growing axon

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internal framework function of the cytoskeleton

positions organelles

Arranged in a defined pattern along an axis from the apical to the basal end of the cell 

Interaction of PROs on an organelle’s surface which adheres to the cytoskeleton

ex: gut –> vesicles are located near the lumen of the gut to prepare for digestion

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how is the intracellular organization disrupted? & what evidence is there?

drugs or mutations that interfere with the normal cytoskeleton structure

Normal: Golgi is packed around the nucleus
Mutation: Golgi is scattered & dispersed

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microtubule structure

tubulin heterodimer composed of alpha & beta subunits

will polymerize to form protofilaments which form a cylinder

protofilaments are asymmetric, alpha at one end & beta at the other

All protofilaments in a single MT have the same polarity

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how many protofilaments are in a cylinder?

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what is responsible for the polarity of the MTs?

beta subunit

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plus end of a MT?

Beta subunit exposed at the end

provides polarity

fastest end of growth (easier to add to the beta end)

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minus end of a MT?

a subunit

slow growth or loss

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gamma tubulin

looks like alpha & beta in size & shape

initiates growth of MTs

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when does gamma tubulin dissociate from MTs?

after polymerization has occurred

once it gets to a certain length, the gamma subunits retract via ATP hydrolysis

regulation of MT stability is dependent on what factors?

Rates of assembly & disassembly are dependent on the local tubulin concentration
More subunits available = quick growth
Polymerization is triggered by having the right amount of subunits (require GTP bound subunits)
Not enough subunits = depolymerization

Stability is dependent on presence of GTP
Enzymes present to replace GDP with GTP to retain stability
GTP hydrolysis reduces the affinity the tubulin has for its neighbor = disassembly

Stability is maintained by continuous addition of GTP labeled tubulin

what controls a MT’s instability?

GTP hydrolysis when bound to tubulin

What does a tubulin dimer require in order to bind to the MT?

bound GTP

what is the effect of GTP hydrolysis on a tubulin dimer in a MT?

reduces its affinity for the tubulin neighbour

how is stability maintained in GDP dimers?

GDP is replaced with GTP

what triggers polymerization?

right amount of subunits (require GTP bound)

what triggers depolymerization of MTs?

not enough subunits available

what type of tubulin can attach to others?

GTP bound tubulin dimer

what happens if MTs are with GDP for too long?

collapse

what provides stability to MTs?

continuous addition of GTP labeled tubulin

how does the cytoskeleton enable cell movement?

rapid assembly & disassembly

how is MT length maintained?

removing tubulin at one end & adding it at the other

How do MT drugs target cancer cells?

Cancer cells require faster cycling of tubulin to facilitate their rapid division Cancer cells lack mitotic checkpoints & continue to divide even in the presence of a drug, but normal cells halt division until the drug is cleared MTs are required for proper c’some segregation, cancer cells divide with improper MTs & produce inviable cells 1 daughter cell will be n & the other 3n

MTOC

growth of MTs are constantly initiated (outwards from the MTOC)

what are the 2 kinds of MTOCs?

2 kinds where basal bodies are assoc with: Base of cilia or flagella Centrosome – creates 2 poles where MTs extend Contain 2 centrioles surrounded by pericentriolar material

pericentriolar material

cloud of PROs surrounding the 2 centrioles in a centrosome contain gamma tubulin

where is the MTOC located in plants?

embedded in the nuclear membrane, lack a centrosome

why do animal cells have centrosome & animals don't?

animal cells are more dynamic & plant cells are more rigid

centrosome structure & what is the total of MTs?

2 centrioles perpendicular to each other surrounded by pericentriolar material 9 fibrils form an outer ring, each fibril is composed of 3 fused MTs + 1 fibril in the middle with 3 fused MTs total of 30 MTs

function of centrioles?

unknown, aren't actually involved in MT nucleation. Recruit the molecules that are involved in MT nucleation can remove centrioles in animal cells & there aren't any adverse effects

function of Tau PRO?

ensures MTs remain parallel with one another

MAPs

MT assoc PRO stabilize MTs (even in the absence of GTP) alter assembly & disassembly rates crosslink adjacent MTs

How is MAP activity controlled?

addition of phosphate on particular AA residues by PRO kinase --> removed from MT removal of phosphate on particular AA residues by phosphatase --> remain on MT

how are MAPs involved in Alzheimer's?

Abnormally high phosphorylation of a MAP, specifically the tau PRO Hyperphosphorylated tau PRO stick together into neurofibrillary tangles in neurons & cause MTs to disintegrate Collapse – short MTs prevent normal intracellular transport & kill the cell leading to brain deterioration Neurons are unable to move their vesicles with neurotransmitters to the periphery

fruit flies with mutated tau PRO exhibit what kinds of defects? & what evidence is there?

neural, motor & cognitive Climbing tests --> motor courtship training - cognitive, females excrete a pheromone when rejecting males after their courting, males don't learn to stop courting & continue to do so neural deformations - neural

MT stability is due to:

abundance of tubulins attachment of GTP MAPs