TA tutorials II Flashcards

1
Q

After shredding marine sponges, the cells are not reforming. What might you add to get the cells to reform?

A) Vitamin C
B) Calcium
C) Talin
D) Actin

A

B) Calcium: Required for Cadherins to bin

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2
Q

Which of these are proteins involved in cell signaling? Choose all that apply.
A) Collagen
B) Integrins
C) G Proteins
D) Adenylyl cyclase
E) Adrenaline

A

BCD

A) Collagen: Provides structural support
B) Integrins: Necessary signaling to let cells know they are attached
C) G Proteins: Critical in signaling pathways
D) Adenylyl cyclase: Common effector molecule
E) Adrenaline: Not a protein

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3
Q

A cell is treated with a drug that limits adenylyl cyclase to producing only ONE cAMP per activation.

Draw a graph comparing the physiological response curve to adrenaline concentration, showing both the fraction of surface
receptors bound to the ligand and the normal physiological response.

A

Somewhere between the
physiological response and fraction of bound surface receptors

  • Multiple Adenylyl
    cyclase and PKAs
    activated even if cAMP
    is repressed
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4
Q

What might be the consequences for a cell which is unable to express Talin/Kindlin? Select all that apply

A) A severely weakened ability to bind to the ECM
B) Polymerization of collagen inside the cell
C) Loss of adhesion signaling
D) Loss of focal cohesion networks
E) Gα proteins will not dissociate from Gβ/Gγ

A

ACD

A) A severely weakened ability to bind to the ECM: Talin/Kindlin help stabilize Integrins
B) Polymerization of collagen inside the cell: Talin/Kindlin not involved with collagen
C) Loss of adhesion signaling: Talin/Kindlin form the start of a signaling pathway
D) Loss of focal cohesion networks: Integrin fundamental to these networks
E) Gα proteins will not dissociate from Gβ/Gγ: Talin/Kindlin not associated with G proteins

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5
Q

Cell-Cell/Cell-Matrix Terms

A

Cell-Cell Adhesions

Cell-Matrix Adhesions

Cell adhesion molecules (CAMs)
-Cadherins :Cis Interactions & Trans Interactions
-Integrins: Tallin and Kindlin
-Adapter proteins
-Laminin
-Collagen IV

Focal adhesion complexes

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6
Q

Short Term Signaling Terms

A

Short Term vs Long Term

Ligand

Adrenaline (Epinephrine)

G protein-coupled receptors (GPCRs)

G proteins
-G α, G β, G γ

Effector

Forster resonance energy transfer (FRET)

cAMP

Protein Kinase A

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7
Q

You are trying to identify the mutation that caused cancer in your patient. You notice that a single growth hormone
has an amplified effect on the growth of cancer. Which of the following mutations could have caused this cancer?

A) Ras is consistently turned on
B) SH2 domain activates for both phosphorylated and non-phosphorylated tyrosines
C) There is an increased number of Receptor Tyrosine Kinases
D) There is an increase in growth hormone releas

A

C

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8
Q

If a mutation were to occur in
each of the following proteins, making them constitutively active, which
would lead to an increased formation of Shmoos in budding yeast? Select all
that apply.
A) Phosphatase
B) Receptor Tyrosine Kinase
C) Sos
D) Ras

A

BCD

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9
Q

How does Ca2+ control the release of
synaptic vesicles?

A

Binds to Synaptotagmin, causing Complexin to displace

(which prevents the synapses from binding with the membrane)

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10
Q

Why are neurotransmitters so small? Select all that apply.
A) Why is anything anything, they’re just like that
B) To facilitate reuptake
C) To facilitate packaging into synaptic vesicles
D) To ensure rapid diffusion

A

BCD

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11
Q

Long Term Signaling Terms

A

Growth Factor

Receptor Tyrosine Kinases

EGF

Ras

GRB2
-SH2 domain

Sos

Shmoos

Kinases

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12
Q

Nervous System 1: Synapses

A

Neurotransmitters
* Synaptic vesicles
* SNARE
* Synaptotagmin
* Complexin
* Symporter
* Dynamin

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13
Q

Why are microtubules necessary for proper Neuronal migration? Select all that apply.
A) Microtubules connect to Rho family of GTPase and perform upstream regulation of Actin

B) Without microtubules, growth cones will extend in all directions and prevent directional movement

C) Microtubules are affected by Semaphorin signaling

D) Microtubules form the growth cone

A

AC

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14
Q

A muscle cell has a mutation which prevents Troponin from binding to calcium. Which of the following is False about this cell?

A) Rigor Mortis could not occur
B) The muscle could not contract
C) The muscle could not relax
D) The Sarcoplasmic reticulum
could release calcium

A

C

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15
Q

You are investigating a mutant
yeast cell which seems unable to
divide. Which of the following
proteins could be mutated?
Select all that apply.
* A) Wee1
* B) Cdc25
* C) Cdk
* D) Cyclin

A

ALL

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16
Q

Describe how muscle cells are able to
execute fine motor movements as well as generate the force required to lift and hold heavy objects.

A

Massively paralleled actin and Myosin
filaments (Sarcomeres), can
produce a lot of force.

Simultaneously, calcium dependent
actin binding allows for precise control of which muscles fire

17
Q

Terms: Neuronal Guidance and Migration

A

Neurites
* Growth Cone
* Doublecortin (DCX)
* Rho
* Rac
* Polyglutamylation
* Netrins
* Semaphorins

18
Q

Terms: Myosin and Muscle

A

Myosin
* Sarcomere
* Sliding filament theory
* Crossbridge cycle
* Tropomyosin
* Troponin
* Sarcoplasmic reticulum

19
Q

Terms: Cell Cycle 1: Checkpoints

A

Cyclin
* CDK
* Wee1
* Cdc25

20
Q

While screening for mutants, you find a cell whose Dynein act more like Kinesin, moving towards the positive end of the microtubule. How might mitosis be affected by this mutation?
A) Microtubules could not be pulled apart
B) The spindle would not form in the centre of the cell
C) New cells would always have aneuploidies
D) The spindle would not form in the correct plac

21
Q

Why are there so many proteins doing similar actions in the kinetochore?

A

Allows specialized small forces through in parallel will be strong enough to
move the chromsomes but not strong enough to break it

22
Q

The Metaphase-Anaphase transition includes many steps with many proteins which only purpose is to regulate a different regulator. What might happen to a cell if Mad2 in open
conformation was able to ubiqulate securin directly?
A) Nothing, evolution just does complicated things sometimes
B) Anaphase could occur with unaligned chromsomes
C) Anaphase could not occur even with aligned chromsomes
D) Separase would be unable to cleave cohesin molecules
E) Aura-B would be always active even under tension

A

B) Anaphase could occur with unaligned chromsomes – Amplification
of signals allows each unaligned chromosome to stop the proces

23
Q

Mitosis Terms

A

Mitotic spindles
* Kinesisn-5
* Kinesisn-13
* Dynein
* Kinetochores

24
Q

Cell Cycle 2 Terms

A

Proteasome
* APC
* Separase
* Securin
* Mad1 and Mad2
* Bi-orentation
* Aurora-B
* p31

25
There is a single mutant cell unable to bind to the ECM of a host. What could be the cause of this mutation? Select the best answer. * A) Pro-peptides are unable to be cleaved from Collagen * B) Kindlin and Talin are unable to bind to integrins * C) Cadherins can no longer become activated by calcium * D) Laminin is no longer produced in focal adhesion complexes
B A) Pro-peptides are unable to be cleaved from Collagen – Affects structural stability not binding C) Cadherins can no longer become activated by calcium – Cadherins part of cell-cell adhesion D) Laminin is no longer produced in focal adhesion complexes – Laminin is not part of FAC
26
At which step of G-protein activation is GTP hydrolyzed to GDP? A) When GPCR binds to a G-Protein B) When GPCR binds to a ligand C) When Gα binds to a effector D) When Gα dislocates from a effector
D
27
Explain how we know the speed in which Gα dislocates from the G- protein complex?
using the FRET (Forster resonance energy transfer) method. FRET involves two molecules, cyan and yellow: If they are very close then the yellow will absorb the light, if they are not, then the light will be cyan. By placing one on Gα and one on Gβ/Gγ, we can measure the light to see the speed
28
Why are receptor tyrosine kinases a cancer-causing agent? * A) Phosphorylates GRB2 when overexpressed * B) Indirectly turns on Ras which is over expressed in 20- 25% of all cancers * C) Part of the pathway to control proliferation * D) Over-expressed in 25% of breast cancers
C
29
Which of the following could be a potential phenotype of a organism with a mutation that turns off Synaptotagmin. Select all that apply. * A) Inability to fire synapses * B) Continuous firing of synapses * C) Inability to reuptake neurotransmitters * D) Inability to package neurotransmitters
A B) Continuous firing of synapses – Mutation in Complexin * C) Inability to reuptake neurotransmitters – Mutation in Dynamin * D) Inability to package neurotransmitters – Mutation in reverse ATPsynthase
30
What is the purpose of a signaling cascade in regard to long term signaling?
By requiring a critical threshold to pass, allows for a switch mechanism
31
Which of the following statements is false? * A) Neuronal stem cells are created in the Stem Cell Microdomain * B) Destabilization of microtubules activates Rac causing lamellipodia formation * C) DCX-KO iNeurons are human neurons with a knockout of Doublecortin * D) Microtubules suppress Rho causing lamellipodia formation
A Its called the Stem Cell Niche
32
At what stage of the crossbridge cycle is ATP hydrolyzed to ADP? * A) Myosin head releases from Actin * B) Myosin head rotates into cocked state * C) Myosin head binds to Actin * D) Myosin head straightens and Actin moved to the left
B
33
At what stage of the crossbridge cycle is ADP released? * A) Myosin head releases from Actin * B) Myosin head rotates into cocked state * C) Myosin head binds to Actin * D) Myosin head straightens, and Actin moved to the left
A
34
How are Wee1 and Cdc25 used to measure the size of a cell in S. pombe * A) The competition of Wee1 and Cdc25 control cell cycle checkpoints * B) Wee1 suppresses CDK through phosphorylation * C) Cdc25 activates CDK by removing phosphates * D) Wee1 indirectly activated by Pom1
D
35
How might Cdc20 cause cancer?
Overactivation of Cdc20 could cause cells to undergo mitosis too rapidly by removing phosphates of CDK and causing it to progress to rapidly through cell cycle checkpoints
36
You find a mutant line with consistent aneuploidies, which of the following proteins could potentially be mutated in this line? Select all that apply * A) Kinesisn-5 * B) Dynein * C) Kinesin-13 * D) Cdc20 * E) CDK * F) p31
ALL
37
Which of the following statements are true? * A) In the presence of Securin, Seperatase inactive * B) Aurora-B is used as an indicator of chromatid attachment * C) Cyclins are degraded by APC * D) Mad2 in open conformation inhibits cdc20 * E) Mad1 is active only when bound to a chromatid
A, B
38
Explain how Wee1, Kinesisn-13 and p31 control the progress of the cell cycle.
Wee1 prevents the overactivation of CDK = preventing the cell from undergoing mitosis too early. Kinesin-13 creates the force necessary to push chromatids apart during anaphase separation. p31 turns Mad2 into the open conformation, eventually snipping cohesion