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MCBG EXAM 3 FINAL > 9-5 Cytoskeleton > Flashcards

9-5 Cytoskeleton Flashcards

0
Q

Size of Microtubules?

A

25 nm

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1
Q

What are the sizes of Actin Filaments

2)These are sometimes called what and where are they usually located?

A

5-9 nm

2)AKA “microfilaments”–>usually located under the Plasma membrane as Cortical Actin

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2
Q

What is the size of Intermediate Filaments?

2)What are these primarily used for?

A

10 nm

2)IF are known for their “physical strength” and are used mechanically often

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3
Q

What Filaments are the Cytoskeleton system composed of?

A

-Highly regulated and dynamic Actin, Microtubules and Intermediate Filaments

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4
Q

What are the 6 Jobs of ACtin (AKA _____)

A

Actin/MICROFILAMENTS)

  1. MAJOR: MUSCLE CONTRACTION (light bands are made of Actin)
  2. Cell Migration/Movement with lamellipodium foot
  3. Cell Adhesion [Adherens junction vs. Focal Contact]
  4. Polarization cell-to-cell
  5. Phagocytosis
  6. CELL SHAPE
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5
Q

Explain why Actin is involved with cell Polarization

A

epithelial cells are polarized within due to Actin anchorage between apical and basolateral membrane compartments

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6
Q

Which filament mediates Phagosome capabilities during Phagocytosis?

A

ACTIN/MICROFILAMENT

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7
Q

What is the process of Cell migration/movement using the ____filament? [2]
B: What r the 3 big uses of this movement?

A

ACTIN FILAMENTS enable cell migration

  • cell polymerizes Actin to the PLUS + end and lamellipodium/cell foot protrudes forward—> foot attaches with focal contact Actin adhesion.
    2) there is then contraction on the myosin II end and cell moves forward along substratum

B: Development / Wound Healing / Cancer Metastasis

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8
Q
  • Actin Filaments have ___subunits assembled in a highly ___process.
  • Explain What Actin Monomers look like and how they’re related to F-actin?
A
  • Actin Filaments have SOLUBLE subunits assembled in highly regulated process.
  • Actn monomer= Globular Actin (G-actin) tht binds to cytoplasmic ATP when free floating.

*Asymmetrical polarized Globular actin (in ATP form) assemble head to tail –forms–> protofilament…2 of these protofilaments wrap around each other–forms—>twisted double helix F-ACTIN FILAMENT

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9
Q

What is the “Ant-Trail” Analogy?

B: why is this important to the overall cell?

A

Filament stick DISassembly into soluble monomers at 1 place and Reassembly of those monomers into a Filament stick in new place
–>looks like moving “ant trail”

B: ULTIMATELY ALLOWS CELL to repolarmerize filaments to diff areas of the cell”such as the lamellipodium foot –>Cell movement!

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10
Q

1) Explain the “lag” / rate determining step of ACtin polymerization?
2) What does the cell do to address this problem?

A

1) There is INITIAL lag for oligomers to bind free Actin soluble monomer subunits into a filament stick via polymerization= rate limiting step

2)Cell overcomes by using
Actin Related Protein Complex(ARP or Nuclei) to mimic oligomers and INSTANTLY start Actin polymerization when/where ever you want

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11
Q

Why is there never NO actual NET change in LENGTH of F-Actin filament sticks?

A

Filament sticks eventually reach EQUILIBRIUM with the concentration of free soluble actin monomers (= Critical Concentration) and is constantly assembling [on +end] and disassembling[- end] together at same time (treadmilling)

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12
Q

Critical Concentration

2)What happens if you go below the CC?

A

the concentration of free Actin soluble monomer subunits at which Filament sticks have stopped growing in length and are at equilibrium!
Different for each filament

2)Going below the CC = SHRINKAGE of the Filament Stick

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13
Q

ARP (___ ____ _______) AKA [ __] allows the cell to….

2) Where can it do this?

A

ARP2 and 3 (ACtin Related ProteinComplex / Nuclei) allows cell to bypass initial polymerization “lag” and start when/where it wants

2) usually activates Actin polymerization at CELL SURFACE but can do it anywhere in cell!

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14
Q

How does [+] and [-] polarization play a role in Actin polymerization?
2) What is CapZ?

3)WHat is Cofilin?

A

Actin polymerization occurs on F-actin [+] end since it is more dynamic AND since [ - ]is more sluggish with higher critcal concentration

2) CapZ caps [+] end of actin filament and prevents premature shrinkage
3) destabilize the [-] GDP end and induces DEpolymerization. Monomers released are RECYCLED on the + end during treadmilling.

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15
Q

What’s the “alternative”/2nd way to carry out Actin polymerization?

A

Thymosin[- end] and Profilin [+ end] binds to free subunits monomers and also carry out F-actin polymerization but this process is LESS EFFICIENT

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16
Q

Which end of F-actin filament has higher Critical Concentration THRESHOLD and why?

2)Why is this even important?

A

[- end] of F-actin filament has “slightly” HIGHER Critcal concentration THRESHOLD–>means it takes more free actin monomers (than what’s actually present) to reach CC for the [- end]—-leads to–> [-] end shrinkage/disassembly becuz it won’t reach CC as fast as +

2)THIS IS WHY YOU HAVE TREADMILLING (+ end assembly and [-] end disassembly)

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17
Q

WHat is the Gel-Actin in the Lamellipodia cell foot?

A

multiple F-actin filament sticks “gel’d” togethr by either

ARP2/3 or [Filament-binding-complexes] (like Filamen dimer) binding the sticks in different angles to form a GEL

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18
Q

What is Fimbrin?

2) why is this a disadvantage for motor proteins?
3) What is an example of this?

A

Monomer w/2 Actin binding domains RIGHT next to each other in same direction/orientation = VERY CLOSE TIGHT PARALLEL BUNDLE

2) Motor proteins like Myosin CAN’T get in becuz it’s too tight!
ex. Microvilli, Filopodium

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19
Q

1) A-Actinin/contractile bundles
2) example?

3)How is this related to myosin?

A

Dimer that spaces out F-actin filament binding domains AND orients them in OPPOSITE directions of one another=ANTIPARALLEL–> (contractile bundle)

2) Found in Stress Fibers(which crosses cytoplasm and surface area) AND MUSCLES
3) space is needed so motor proteins like myosin can move along the spaced out F-actin filament sticks

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20
Q

Terminal Web

A

Location where [actin gel-arrays] join w/cortical actin under PM and help anchor membrane protrusion into the cell

(how microvilli is planted into the cell)

21
Q

How does Actin-based drugs work?

2)What is an example of this drug and does it have a positive usage?

A

TOXIC drugs bind to F- filaments in multiple places and STABILIZE
F-ACTIN FILAMENT STICKS–>disrupts normal polymerization!

(ex. Phalloidin from the DEATH CAP MUSHROOM)
- also are powerful tools in lab to stain and understand ] Actin
- –>reduces the Critical Concentration threshold to zero! –>Actin will always keep growing and growing and growing at ANY free actin monomer concentration

22
Q

Global Actin Rearrangement includes these. Describe:
1) Rho - GTPase

2) Rac Rho
3) Cdc42 Rho

A

1) fibrin biochemical switch that creates AnTi-Parallel Actin stress Fiber organization in active (GTP form)
2) GTPase that creates Lamellipodia/Membrane Ruffles or “curtains” and is often seen a lot in migrating cells
3) makes TIGHT Parallel bundles of ACtin like Filopodia or MICROSPIKES

23
Q

How do Bacterial toxins target actin polymerization?

A

disrupt actin polymerization by messing with Rho GTPase Family—->

  • cell death
  • tight junction problems/diarrhea
  • DEC in cell integrity
24
Q

What happens if you INC the free actin monomer concentration ABOVE the critical concentration threshold?

A

The F-filament stick will began to grow!

25
Q

What does Phalloidin drug do when you DEC free actin monomer subunits to low low number?

A

Even if you dilute out all the free actin monomer subunits to low # the F-actin filament stick IS STILL STABILIZD[Critcal concentration threshold=0] due to Phalloidin and WONT DISASSEMBLE like normal F-actin would

26
Q

Describe Myosin II

A

Myosin II dimer motor protein
(2 Long coiled helix tails with N-terminal power head)
*a-helix tails overlap in the bear zone and ultimately form bipolar (head pointing in diff directions) THICK Filament

*Move toward the + end (more common) or move toward [-] end

27
Q

how do you get muscle contraction?

A

ATP DEtaches myosin bipolar THICK heads from ACtin and then ATP hydrolysis causes myosin 2 “cock back”

  • –(Phophate release)–>myosin rebinds stronger to actin
  • —ADP release—>power stroke moving multiple actin toward [+ end] of other opposite pointed actin!=Rigorous state

These myosin bipolar thick heads work rapidly and independently!

28
Q

Rigorous State

2) How is ATP related to the Rigorous state and muscle contrction?

A

Rigorous=ATP is ABSENT and all myosin heads are bound to Actin thin filament contracted

29
Q

Familial Hypertrophic Cardiomyopathy

A

Myosin Beta heavy chain mutations can cause Enlarged Heart, Cardiac arrhythmia and Sudden Death of young athletes!

30
Q

Microtubules

2)What are 5 big functions?

A

can be near nucleus (Microtuble organizing centers)

  1. positioning organelles
  2. cell anaphase division [mitotic spindles]
  3. enable inner cell vesicle movement (from ER->Golgi, etc. )
  4. Cell motility [sperm,protozoa via flagella]
  5. Cilia in respiratory tract

(ex. Golgi kept near Nucleus)

31
Q

Describe the structure of Microtubules

A
  1. soluble subunits are a-tubulin and b-tubulin dimers binds to GTP
  2. 13 protofilaments in a hollow straw “slurpy straw”
  3. Rigid and highly polar
  4. [-] end burried in microtubule organizing center(centrosome most common) STABILIZES IT and so this is why no addition or subtraction going on at the [- end]
32
Q

Microtubule Organizing Center

A

in centrosome there are gamma-tubulin ring complexes (similar to ARP2/3 or nuclei of the Actin filaments)that ultimately pushes centrosome toward center of cell near nucleus because it polymerizes microtubules in a spherical pattern outward. [-] ends are burried within.

33
Q

1) What happens if you hydrolyze the GTP cap on microtubules?
2) How does the cell “Rescue” this?
3) Why doesn’t this affect the [-] end of microtubules?

A

hydrolyzing [+ end] GTP cap (mistakenly happens over time)–>
GDP tubulin dimers alone –(changes)–>normally stable microtubule subunit
into a CATASTROPHE! with rapid depolymerization @ the [+ end]

2) GTP bound subunits will add on to subunits and have growth which will lead to growth and shrinkage back-and-forth over time=Dynamic Instability
3) won’t affect [-] end because it is protected within the centrosome sphere

34
Q

MAPs? [ 2functions]

2) How is tau related to Alzheimers Dz?

A

A. Give spacing between microtubules
[BIGGR SPACED MAP2 vs. shrtr tau]
B. Stabilize microtubules

2) tau MAP protein when hyperphosphorylated–(leads to)–> Neurofibrillary Tangles–(causes)–>Alzheimers Dz [neuron death]

35
Q

Is shutting off Dynamic Instability ok?

A

NO! Interfering with Microtubule Dynamic Instability (ability of filament to grow and shrink) is BAD! it needs this!

36
Q

What is the negative side of using Microtubule-targeted cancer drugs?
example?

A

it targets ANY rapidly proliferating cell using microtubules to grow (skin, hair) and has many side effects

-they are MORE clinically used than actin drugs though
Ex. Taxol = stabilizes microtubules and prevents mitosis

37
Q

1) Kinesins vs. Dyenin?

2) What is axonemal dyenin?

A

Kinesis move stuff toward the + end of microtubules–>involved in carrying out ER—>X transport

Dyenins retrograde move toward [-] end microtubules
[axonemal dyenin move specifically in cilia and flagella]

38
Q

How is microTUBULE motor movement diff. than microfilament?

A

MCT dimers have Each bipolar head in contact with the ACtin filament 50% of the time [not rapid or independent] and work with each other = SLOWER but more stable long-acting movement–>HIGH PROCESSISIVITY

39
Q

What is the internal structure of Flagella & Cilia [2]

A

Cilia and Flagella have axonemal dyenin
1 WHOLE dublet with 9 Microtubule Dublets inside each surrounded by 2 microtubule singlets

2)FLagella=SPerm and PRotozoa=WAVE-LIKE MOTION
Cilia= Respiratory Epithelium= whip-like motion

40
Q

Basal Body structure [purpose and structure]

2) where is this typically located?

A

Anchors Flagella and cilia into cytoplasm and consist of 9 microtubule triplets with no center pair of singlets microtubule (VERY similar to what is in a centriole of a centrosome)
2. LOCATD NEAR THE PLASMA MEMBRANE!!!

41
Q

Kartagener’s Syndrome

2)Sx?

A

defect in ciliary dyenin motor protein RESPONSIBLE FOR cilia and flagella to move
2) Male sterility and Respiratory infections

42
Q 
Intermediate Filaments (AKA \_\_\_ filaments) 
2) where are they common
A

Intermediate Filaments (AKA Kerotinocytes)= Express a lot of Keratin and important for giving mechanical strength to cells. Are abundant in tissue tht withstand a lot of physical beat down (heart, muscles, skin)

  1. Cell strength
  2. cell-to-cell adhesion brtween cytoskeleton and adjacent cells via desmosomes that connect them
43
Q

Neurofilaments purpose and it’s relation to ALS?

A

Intermediate Filament tht Determines Axon diameter and if unregulated can become clustered in brain–>Leu Garrets dz / ALS [ Amyotropic Lateral Sclerosis]

44
Q

Nuclear Lamina

A

Beneath nuclear envelope, this intermediate filament structure gives nucleus its shape

45
Q

What are some KEY characteristics to note regarding Intermediate Filaments? [4]

A
  1. 2 dimers of bipair coiled protofilaments come together in an anti-parallel fashion to make SYMMETRICAL soluble tetramer subunit.
  2. Non-Polar Filament! [very diff from the other filaments!]
  3. VERY strong structure
  4. Very Heterogenous [HUGE gene family-DIVERSITY w/TISSUE SPECIFIC expression]
46
Q

Tonofilaments

  1. Where could this be found?
  2. What helps it
A

Bundle of cytokertain Intermediate Filaments tht interact at
C-terminal domains with each other
2. Skin
3. Plectin and Filaggrin[Filament Aggregation] accessory proteins bind to this bundle

47
Q
  1. Musculary Dystrophy with Epidermolysis Bullosa Symplex Cause?
  2. What is Plectin?
  3. [ 3] associated sx?
A

Caused by Dz in Plectin [universal linker dimer connecting
Vilmentin IF, Actin &Microtubules –> maintains mechanical cell integrity] .

–3–
-EBS (blistering dz due to defect in Intermediate Filaments)
-Neurodegeneration (defect in neurofilaments)
-Muscular Dystrophy (defect in Desmin)
Pt have ALL 3 SX!

48
Q

What are the 4 TYPES of Intermediate Filaments being that IF is extremely _____ (list Name, polypeptide and cell location)

A

Intermediate Filaments are HETEROGENOUS(Huge Gene diversity)!
1. Nuclear=Lamins/Nuclear Lamina–if DFcT—>Progeria

  1. Vimentin-like= Desmin/Vimentin–loctd in->muscle and glial cells
  2. Epithelial= Kertain IF–loctd in–> hair, nail and epithelial
  3. Axonal=Neurofilament–loctd in–> Neurons
49
Q

How can we Use Intermediate Filaments to determine origin of cancer?

A

Intermediate Filaments gene DNA is soo specific to a specific tissue that if cancer cell metastasized/transloctd and you stain for the IF in it you will know where it came from

51
Q
  • Desmosomes

2) HEMI-desmosomes?

A

Intermediate filaments used in Cell-Cell Adhesion

2)HEMI-desmosomes=Cell-MATRIX Adhesion

52
Q

Flagella & Cilia both have ____singlets surrounded by ___ doublets.
2) These two connect to a cell body via the [basal body] which itself is made of ___ ______

A

Flagella & Cilia both have 2 singlets that are SURROUNDED by 9 doublets.
2)They connect to cell body via [basal body] which itself is made of 9 TRIPLETS! smh

MCBG EXAM 3 FINAL (9 decks)

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