Cytoskeleton Part I (24) Flashcards
what are the 3 types of cytoskeleton fibers?
microtubules
intermediate filaments
microfilaments
microtubules
hollow & rigid cylindrical tubes
made of tubulin
responsible for movement from the interior to the exterior & vice versa, but not to the periphery
which fiber is the largest of the cytoskeleton components?
microtubules
What fiber offers the greatest amount of strength & durability?
microtubules
microfilaments
solid, thinner structures
made of actin
intermediate filaments
tough, ropelike fibers
made of a variety of related PROs
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
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)
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
what type of cells are capable of independent locomotion?
sperm
white blood cells
fibroblasts
highly motile tip of growing axon
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
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
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
how many protofilaments are in a cylinder?
13
what is responsible for the polarity of the MTs?
beta subunit
plus end of a MT?
Beta subunit exposed at the end
provides polarity
fastest end of growth (easier to add to the beta end)
minus end of a MT?
a subunit
slow growth or loss
gamma tubulin
looks like alpha & beta in size & shape
initiates growth of MTs
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
