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1
Q

4 phases of cell cycle

A

G1, S, G2, M

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2
Q

true or false?

A

TRUE

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3
Q

Describe what happens at prophase (3)

A

Prophase

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4
Q

What happens at prometaphase?

A

Prometaphase

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5
Q

Describe metaphase

A

Metaphase

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6
Q

Describe anaphase

A

Anaphase is pulling apart of sister chromatids.

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7
Q

Describe telophase (2)

A

•Telophase

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8
Q

Describe cytokinesis: (2)

A

•Cytokinesis

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9
Q

Just read

A

okay

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10
Q

Metaphase is a ___________ phase bc as soon as fully done, anaphase occurs

A

transient

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11
Q

What is the key entry point of mitosis and what is it dependent on?

A

The key start point of mitosis is NEB and it is highly dependent on cdk1-cyclin B

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12
Q

Describe how cdk1-cyclin B causes NEB?

A
  • phosphorylation of nuclear lamins –> disassembly of nuclear lamina –> nuclear envelope breakdown
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13
Q

what other activities are dependent on CDK1-cyclin B activity?

A

Assembly of mitotic spindle and capture of chromosomes by spindle microtubules depends on Cdk1-cyclin B activity

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14
Q

Therefore, NEB, mitotic spindle assembly, and spindle attachment are all dependent on cdk1-cyclin B. true or false?

A

TRUE

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15
Q

What requires cdk1 inactivation? Explain.

A

Spindle elongation and separation of sister chromatids in anaphase require inactivation of Cdk1.

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16
Q

Explain how cdk inactivation occurs and what it is necessary for (2):

A

•APC/C (Anaphase Promoting Complex/Cyclosome) ubiquitinates cyclins –> leading to cyclin destruction –> inactivation of Cdks

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17
Q

What are the 2 approaches to studying the cell cycle?

A

•Genetic screens in S. cerevisiae and S. pombe –> genetic

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18
Q

Describe the genetic screen experiments that were done on yeast cell cycle

A
  • large-scale mutagenesis and screen for temp sensitive mutants (cause protein to not fold properly but at lower temps, will fold properly, but increasing temp will prevent folding and give mutant phenotype)
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19
Q

Yeast ts-mutants can be isolated that arrest cell division with a morphology corresponding to a specific stage in the cell cycle. true or false?

A

TRUE

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20
Q

What does a metaphase arrest result from? (general statement)

A

gene required for anaphase is mutated

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21
Q

What does a late anaphase arrest result from? (general statement)

A

gene required for cytokinesis is mutated

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22
Q

What specifically were the important results found in the yeast study of arrest?

A

One gene important in pombe - cdc2

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23
Q

Describe the procedure that was done to determine the gene that caused the cell cycle arrest in S. pombe:

A

•S. pombe cdc2 = G2/M regulator

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24
Q

Describe cloning of the S. cerevisiae cdc28 (G1/S regulator)

A

Genetic screens in S. cerevisiae identified the cdc28 gene, required for G1/S

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25
Q

Just read

A

okay

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26
Q

Lil more reading

A

okay

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27
Q

They started just calling cdc28 and cdc2 as what?

A

CDK1

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28
Q

Describe how they determined that CDK1 is a kinase?

A

•in vitro kinase assay

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29
Q

So, describe the experiment that they did that shows the cyclic activity of CDK1:

A

-synchronize yeast cells (Hydroxyurea block then release)

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30
Q

True or false?

A

TRUE

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31
Q

Reading is for champions. Are you a champion?

A

Yes

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32
Q

How are mitosis and meiosis similar?

A

•entry into meiosis - NEB (aka maturation) - is similar in many respects to entry into mitosis

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33
Q

•meiosis II is very similar to a mitotic division (sister chromatids segregate)

A

homologues

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34
Q

Describe how meiosis is regulated:

A

-prophase –> NEB (progesterone)

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35
Q

meiosis is followed by what?

A

zygote formation and specialized rapid mitotic cell divisions (early embryo)

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36
Q

___________ causes nuclear breakdown, meiosis progresses until metaphase II and the ___________ triggers completion of meiosis and you get rapid mitotic divisions of embryogenesis

A

oocyte

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37
Q

Describe meiosis regulation

A

Oocytes arrest in prophase of meiosis I until Progesterone triggers maturation.

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38
Q

Remains in meiosis II until what?

A

Remains in meiosis II until fertilization

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39
Q

Describe the experiment that started the biochemical approach to cell cycle and what important component of regulation it introduced

A

-Remove cytoplasm from mitotically cycling embryos (eggs that have been released from meiosis II arrest by fertilization or in vitro activation)

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40
Q

Describe the experiment that showed cyclic character of MPF

A

•1977 - Cytoplasm taken from embryos at given times before or after activation - has different abilities to induce maturation in arrested oocytes.

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41
Q

He also took cytoplasm from ________ arrested, inject into immature oocyte and could promote maturation

A

csf

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42
Q

Explain how the cyclic nature of MPF was proven to require protein synthesis

A

•Cycloheximide (blocks protein synthesis) added to dividing embryo leads to arrest before nuclear envelope breakdown (prophase arrest).

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43
Q

True or false?

A

TRUE

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44
Q

Describe the identification of cyclin B

A

35S-Met added to eggs to label all proteins.

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45
Q

Describe CSF arrest and CSF extracts:

A

CSF arrest: after completion of meiosis I, eggs enter meiosis II and arrest in metaphase.

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46
Q

Describe the in vitro mitotic cell cycle using CSF extracts and how it showed the necessity of cyclin B for entry into mitosis:

A

•Production of cycling extracts: cytoplasm from CSF arrested eggs + sperm nuclei + ATP + Ca2+

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47
Q

How did the yeast work and cyclin work come together?

A

•1989 -Affinity purification of Cdk1 from starfish oocytes. Cyclin B copurifies.

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48
Q

So they co-purified and MPF was identified as cdk1-cyclin. True or false?

A

TRUE

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49
Q

Name the different cdk-cyclin pairs that are active at different phases of the cell cycle:

A

G1 CDK –> CDK4-CyclinD or CDK6-cyclinD

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50
Q

All Cdk’s are ___________ kinases that depend on a cyclin partner for activity and specificity.

A

Ser/Thr

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51
Q

Describe the process of activation of CDKs: (4)

A

1.cyclin binding

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52
Q

So describe the multi-functionality of CDK7

A

So cdk7 has multiple important roles, it phosphorylates CTD of RNA pol II and phosphorylates cdk1 and cdk2 in order to activate them

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53
Q

Describe wee1 kinase

A

Wee1 kinase is an inactivating kinase, so the phosphorylation from wee1 kinase inactivates cdk, so it needs to be removed from cdk for activation (cdc25 phosphatase does this)

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54
Q

Describe the positive feedback loop of CDK1:

A

Positive feedback loop occurs because active cdk can phosphorylate cdc25 and wee1.

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55
Q

Prophase events

A

•chromosome condensation.

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56
Q

Events of prophase all occur bc of cdk1 and then a critical level is reached that allows for __________

A

segregation

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57
Q

in Prophase:

A

Condensin forms a ring that is thought to loop together parts of the same chromosome to condense it.

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58
Q

Explain why interphase chromosomes are decondensed, why prophase are condensed, and describe what is needed for condensation:

A

•Interphase chromosomes are decondensed - allows for transcription and for DNA replication at S-phase

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59
Q

Prometaphase events

A

•nuclear envelope breakdown (NEB)

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60
Q

Describe nuclear envelope breakdown

A

•NEB is the key initiating event of mitosis.

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61
Q

True or false?

A

TRUE

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62
Q

Describe the mitotic spindles (characteristics and types):

A

They are polar, having a minus end at the centrosome and plus end that goes out

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63
Q

What is this?

A

Astral microtubules

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64
Q

What is this?

A

interpolar microtubules

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65
Q

What is this?

A

kinetochore microtubules

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66
Q

Replicated sister chromatids are held together by __________.

A

cohesins

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67
Q

Separation of sister chromatids requires loss of _____________ and pulling of kinetochore microtubules

A

kinetochore

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68
Q

Centromere of chromosome binds to kinetochore proteins which binds to spindle. True or false?

A

TRUE

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69
Q

Describe kinetochore attachment and the shortening of the spindle

A

Kinetochore attachment:

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70
Q

In prometaphase, kinetochore attachments are ____________.

A

unstable

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71
Q

Read over WELL

A

okay

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72
Q

Define the following: monotelic, syntelic, and merotelic:

A

monotelic - single attachment

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73
Q

Describe how bipolarity is ultimately established in mitosis:

A

Proper segregation requires capture of both sister chromatids by microtubules from the opposite poles (amphitelic attachment).

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74
Q

Read over well

A

okay

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75
Q

Why do chromosomes remain at the midzone during metaphase?

A

In metaphase, chromosomes remain at the midzone because they are attached to each other via cohesins.

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76
Q

Why does anaphase occur? What does this require?

A

Anaphase occurs when cohesin bonds are broken.

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77
Q

•Destruction of ____________ and ____________ depends on a ____________ ____________, the ____________

A

securin

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78
Q

What showed that cyclin B gets degraded?

A

Add 35-S-CycB (radioactive labeled Cyclin B) in the in vitro mitotic cell cycle

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79
Q

How did they identify the sequence for degradation (destruction sequence)?

A

Make deletions from N-terminus –> assay for degradation in cycling extract

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80
Q

they got rid of first 90 Aas from N-terminus end resulted in non degradation, so something there was important. true or false?

A

TRUE

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81
Q

What did they notice about the non-degradable cyclin B (delta90CycB)? Explain the significance:

A

The extract arrests in mitosis (Early anaphase)

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82
Q

So, this arrest was not because it was non-functional. It was its presence when it should’ve been broken down that caused the arrest. True or false?

A

TRUE

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83
Q

What happens if you add both delta90 and normal cyclin B?

A

The normal cyclin B gets degraded, but arrest still occurs.

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84
Q

When a cycling extract has CycBD90 added:

A

mitotic extract

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85
Q

True or false?

A

TRUE

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86
Q

So summarize what happens if you deleted first 90 AA of cyclin B:

A

-still able to induce entry into metaphase in Xenopus extracts or eggs

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87
Q

List the 3 aspects of CDK-cyclinB that have been covered:

A

•MPF (Cdk1-cyclin B) is necessary for entry into mitosis.

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88
Q

How can you determine what sequence within the 90 aa is important for cyclin destruction?

A

-look for conserved motifs within this region amongst cyclins from different species.

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89
Q

After they found the destruction box, indicate what 2 things they needed to find out about the sequence and how they found them out:

A

•Determine that this sequence is necessary and sufficient to mediate cyclin B destruction.

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90
Q

What happened to protein A when fused with the destruction box? Explain what was seen on the gel and the meaning.

A

Protein A fused to destruction box is destroyed over time.

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91
Q

get slide 79 of lec15-16 ?

A

okay

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92
Q

Explain the relationship between cdk-cycB and the APC

A

the cdk cyclin B activates the APC, which targets the cyclin for destruction, thereby inactivating cdk

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93
Q

How is the cdk-cycB and APC interaction affected if mitotic extract is used (delta90 cycB or mutation)?

A

In a situation where cyclin B is incomplete (missing 90 Aas or has a mutation), it is still active in that the cdk can still phosphorylate APC because it can still interact with cyclin B, but it cannot be degraded because destruction box is missing or mutated, so it cannot be ubiquitinated and thus degraded. So, CDK activity keeps up, but APC degradation of cyclin cannot occur despite being active.

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94
Q

Summarize the process of Cyclin B cycling and mitosis:

A

•Cdk1-cycB promotes NEB and other events of mitosis

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95
Q

How do we get a cycling of active and unactive APC?

A

Remember, because you get degraded cyclin as a result of active APC, you no longer have cdk activity, meaning you lose APC activity. This makes the cycle.

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96
Q

____________ must be destroyed for late anaphase to proceed

A

securin

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97
Q

When are cohesin complexes assembled?

A

s-phase

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98
Q

Cohesins keep sister chromatids together until ______________ of mitosis

A

anaphase

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99
Q

Describe sister chromatid cohesion:

A

•During DNA replication (S-phase), cohesin complexes assemble and keep sister chromatids together.

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100
Q

_______ is important bc it is the subunit (of cohesion) that is proteolytically cleaved during anaphase - cut in half

A

scc1

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101
Q

Key event of anaphase:

A

cleavage of scc1 protein (removal of cohesin ring allows for sister chromatid separation)

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102
Q

3) delta90 Cyclin B

A

1) 2 sister chromatids are separated to the daughter nuclei

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103
Q

Molecularly, what happens during anaphase to get separation of sister chromatids? Start with sister chromatids being together.

A

Sister chromatids together bc of cohesin

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104
Q

Indicate when APC mutants arrest and the state of the chromosomes:

A

APC mutants arrest in metaphase with sister chromatids still associated

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105
Q

Indicate when stabilized cyclin B arrests and the state of the chromosomes:

A

•stabilized cyclin B results in arrest with sister chromatids separated (early anaphase - cannot proceed to late anaphase)

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106
Q

What happens in securin mutants?

A

Securin mutants mean that you get active separase when you shouldn’t, meaning you get faulty and premature separation (before anaphase)

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107
Q

What happens securin D-box mutants?

A

•D-box mutant of Securin results in failed sister chromatid segregation, just like APC mutants.

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108
Q

The main function of APC is to target __________, and the main purpose of __________is to prevent anaphase

A

securin

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109
Q

3) APC/securin double mutant

A

1) would look just like WT, separated chromatids because separase would prematurely separate before anaphase

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110
Q

Explain why APC/securin double mutant gets separation AND arrests in late anaphase:

A

Separation makes sense because securin mutation means it premature separation as a result of active separase

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111
Q

Securin prevents anaphase by protecting ________. APC promotes anaphase by promoting Securin destruction.

A

scc1

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112
Q

3) APC/securin double mutant

A

1) No because got degraded by separase

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113
Q

How did they discover separase?

A

Took securin protein, fused it to beads and identified proteins that can bind to it (like a Co-IP). They found separase

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114
Q

What did separase mutant show?

A

no separation, looks like APC mutant!

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115
Q

true or false?

A

TRUE

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116
Q

Describe what is expected from a separase/securin double mutant

A

looks like separase mutant (or APC mutant) because securin is only needed to inactivate separase, which is not active bc of the mutation

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117
Q

Mutants with stabilized scc1 arrest where?

A

metaphase

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118
Q

Briefly indicate the Securin, Scc1 and Separase interactions

A

•Prior to anaphase securin binds to and inhibits separase.

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119
Q

What keeps the APC inactive?

A

Spindle assembly checkpoint (SAC)

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120
Q

Describe the introductory experiment to the SAC

A

•Treatment of cells with colchicine or vinblastine (microtubule destabilizing drugs) or with taxol (microtubule stabilizing drug) leads to a mitotic arrest. Cdk activity is high, cyclin B and securin are stable.

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121
Q

Describe how the Spindle Assembly Checkpoint works:

A

•The APC is kept inactive until all kinetochores have made stable connections to spindle microtubules from both poles.

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122
Q

As proper attachment occurs, SAC is inactivated at that kinetochore. True or false?

A

TRUE

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123
Q

Mad2 is activated when SAC is activate (it is a part of SAC), promotes the inhibition of what?

A

cdc20 of APC

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124
Q

SAC is recruited to what?

A

unattached kinetochores

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125
Q

How does mad2 work?

A

•Mad2 component of SAC is recruited to kinetochore, activated, released.

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126
Q

Describe the kiss and run model of sac:

A

Mad2 cycles off of kinetochores as long as it is not occupied

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127
Q

true or false?

A

TRUE

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128
Q

Describe what happens in prometaphase, then metaphase, then anaphase as a result of APC/C and SAC activity

A

In prometaphase, some chromosomes are properly attached while others are still unattached or have monotelic attachments

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129
Q

Run through diagram on slide 98 of 15/16

A

okay

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130
Q

slide 100

A

okay

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131
Q

As microtubules gets shortened, it stays attached, causing pull force that drives anaphase B

A

collar

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132
Q

Anaphase is initiated by ___________ mediated destruction of ___________ and ___________

A

APC/C

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133
Q

Describe what initiates anaphase A and B respectively and what they result in:

A

•Anaphase A - Securin destruction –> loss of cohesion - pulling forces of kinetochore microtubules partially separates sister chromatids

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134
Q

What does this describe?

A

cytokinesis

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135
Q

Describe the midbody in cytokinesis:

A

Cytokinesis continues until a thin bridge connects the two cells. This contains remnants of the central spindle, actin/myosin and matrix material.

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136
Q

Important for determining where cytokinesis occurred in the first place.

A

Interpolar microtubules

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137
Q

________________ _________________ release signal that instruct cytokinesis to occur at this site

A

Interpolar microtubules

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138
Q

Them together pulls the membrane together

A

actin

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139
Q

myosin II in contraction of non-muscle cells:

A

Myosin is a motor protein

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140
Q

Motor activity of myosin brings membrane closer together. true or false?

141
Q

There are different models for how the contractile ring is established. There is good evidence for one in which the _____________ _____________ (_____________ _____________ ) sets up the contractile ring

A

central spindle (spindle midzone)

142
Q

How does the central spindle play a key role in contractile ring formation of cytokinesis?

A

Determining where contraction occurs

143
Q

__________ is essential for the assembly of the actin/myosin contractile ring

144
Q

Describe RhoA

A

RhoA - activated near central spindle (interpolar microtubules)

145
Q

Describe the experiment result that proved RhoA recruits actin and myosin to the contractile ring

A

WT cell undergoing cytokinesis

146
Q

Describe the latrunculin A experiment (depolymerization of actin):

A

Drug depolymerizes actin and prevents cytokinesis (no pinching seen)

147
Q

Describe myosin heavy chain (MHC) RNAi knockdown result:

A

Cell doesn’t form cleavage furrow

148
Q

What did the latrunculin A and MHC knockdown experiments conclude?

A

actin and myosin are both necessary for cytokinesis, but RhoA is in an upstream pathway of actin and myosin because it doesnt depend on them being present for it to be present.

149
Q

What is ECT2?

A

The GEF for RhoA –> promotes its active GTP-bound state

150
Q

Actin and myosin localize at the site of cleavage, but ECT2 actually localizes to the overlapping interpolar microtubules at the central spindle (spindle midzone). True or false?

151
Q

What is the fate of ECT2 RNAi cells?

A

failure to undergo cytokinesis

152
Q

What is ETC2 necessary for?

A

RhoA accumulation at the contractile ring (localization of RhoA)

153
Q

Provide the full pathway for mitotic spindle dependent contractile ring assembly:

A

•CYK-4 associates with the mitotic central spindle

154
Q

Describe CYK-4 role and studies:

A

CYK-4 is necessary for cytokinesis and for localization of MHC, actin, ECT2 and RhoA.

155
Q

Describe the experiment that answered the following question. “How is RhoA activation regulated so it is active only after mitosis?”

A

Start with cells synchronized in metaphase at time 0

156
Q

State what they found to be the thing that stops the binding between ect2 and cyk4 and why it makes sense:

A

Cdk1 phosphorylation stops the binding, which makes sense because in anaphase cdk1 is degraded, which means that the binding can occur in anaphase, allowing for activation of RhoA

157
Q

ECT2 immunoprecipitates CYK-4 in _____________.

158
Q

Phosphorylation of ECT2 (pTP) correlates with ability or inability to bind?

159
Q

Therefore Cdk1 phosphorylation of ECT2 prevents recruitment of ECT2 to the spindle midzone. Anaphase cyclin destruction permits ECT2 recruitment. True or false?

160
Q

get slide 17 info from lec 17-18

161
Q

Summarize the model for RhoA activation at the contractile ring:

A

•CYK-4 associates with the mitotic central spindle (interpolar microtubules that don’t associate with stuff)

162
Q

In g1 of cell cycle, what complex is formed and what 2 kinases are a result of its formation (provide what the kinases do in the context too)

A

Prereplicative complex forms (preRC)

163
Q

In order of appearance in the cell cycle, name the CDK/cyclin pairs that pertain to each phase or checkpoint and what they are inhibited by:

A

•G1: Cdk4/cyclinD (inhibited by INK4)

164
Q

Which cdk cyclin pair needs to be activated for S to occur?

A

Cdk2/cyclin A

165
Q

Describe what happens in embryonic cells meiosis and mitosis with no G1 phase in terms of cyclin and APC:

166
Q

What happens in cells with G1 phase (normal cells) in regards to their cyclin and apc in M and G1:

A

Cells that have a G1 phase

167
Q

Describe the relationship between the types of APC

A

apc/c-cdc20 gets phosphorylated to be activated, but then it gets inactivated and APC/C-cdh1 comes along as the first goes down because they are oppositely regulated by phosphorylation

168
Q

What are the reasons for low cdk activity in g1? (3)

A
  • cdh1-APC/C is active, which keeps m-cyclin (cyclinB) level low
169
Q

•________ inhibits Cdk4-cyclinD

170
Q

-•Cells that are terminally ___________ (most cells in our body) arrest permanently in a G1-like state - referred to as ___________

171
Q

The decision whether to enter S phase is coupled to what?

172
Q

•All cells have some mechanism of coupling cell division and growth. Briefly explain this in unicellular and multicellular organisms:

A

•In unicellular organisms the main determinant of rate of division is nutrient availability for that cell.

173
Q

•In most cells, the decision of when and if to divide is made in ________ of the cell cycle

174
Q

Entry into S-phase involves what sequential activation?

A

G1-Cdks –> G1/S-Cdks –> S-Cdks

175
Q

rate of cell division must be coupled to rate of cell growth

A

protein synthesis

176
Q

In S. cerevisiae, nutrients entering the cell activate what pathway? List what this pathway generally promotes (not just in yeast):

A

TOR kinase

177
Q

Describe Growth and Cell cycle control in budding yeast starting from the accumulation of nutrients in the cell:

A

•low nutrients –> yeast cell makes less proteins and does not divide.

178
Q

Explain specifically why S phase is so dependent on nutrients levels/growth:

A

•The G1 cyclin Cln3 is very unstable (constantly subject to ubiquitin-proteasome degradation) AND its translation is inefficient.

179
Q

get slide 31 info from lecture 17-18

180
Q

•Many mitogens are also ____________ ____________.

A

•In multicellular organisms both growth and the cell cycle are highly regulated.

181
Q

Get info from slide 32 lec 17-18

182
Q

and 33

183
Q

Many mitogens such as _________ and _________activate the __________________ pathway.

184
Q

Describe the Ras/MAPK pathway and how it is involved in control of growth and cell cycle

A

Receptor binding by mitogen (ex. pdgf, egf)–> transphosphorylation

185
Q

Just read

186
Q

Myc and fos promote activity of what?

A

G1-CDK activity

187
Q

Myc and fos promote G1-Cdk activity. Explain:

A

•Mitogen signaling leads to transcription of myc and fos.

188
Q

G1-Cdk activity promotes G1/S. Explain:

A

•Cdk4-cyclin D binds p27, helping to relieve inhibition of Cdk2-cyclin E.

189
Q

Mitogens and Cdk4/cyclin D inhibit p27, helping to relieve inhibition of Cdk2/cyclin E. How does cyclin E get further promoted?

A

-Cdk4-cyclin D sequesters p27, allowing low level activation of Cdk2-cyclin E

190
Q

What is the no turning back point for S phase?

A

Mitogens promote activation of the E2F transcription factor

191
Q

get slide 44 info (lect17-18)

192
Q

What is responsible for a rapid increase in levels of G1/S and S-cyclins?

A

E2F1 and other activator E2Fs

193
Q

•In G0 and G1, E2F1 is kept inactive by binding to ________ .

194
Q

G1-Cdks promote S-phase by activating E2F1. Explain this process:

A

•Mitogens promote Cdk4-cyclin D activity and low levels of Cdk2-cyclin E activity (by sequestering p27).

195
Q

Describe activation of the S-Cdk, Cdk2-cyclin A:

A

•E2F1 promotes high level transcription of itself, cyclin E and cyclin A.

196
Q

Provide a summary of the G1 to S transition in higher eukaryotes:

A

•mitogens activate ras/MAPK pathway leading to myc, fos transcription.

197
Q

Describe growth and cell cycle control in yeast vs higher eukaryotes

A

•In yeast the major cue for growth is nutrient levels and the cue for cell division is growth.

198
Q

Describe how replication is initiated in terms of the molecular recruitment that takes place:

A

ORC recruits Cdc6

199
Q

What are the roles of CDK2-cyclin A and DDK and what do they result in?

A

S-Cdk = Cdk2-cyclin A

200
Q

True or false?

201
Q

Briefly describe the status of DNA replication in terms of before during and after S phase (3):

A

•pre-replication complex (preRC) formation in G1

202
Q

Describe the process of BrdU incorporation and what it shows us:

A

BrdU Incorporation

203
Q

•Pre-RC assembly is inhibited after __________ to ensure that ______________ does not occur.

204
Q

What would happen if re-replication wasn’t stopped by inhibiting Pre-RC assembly after S-phase?

A

re-replication would result in tetraploidy - frequently a first step in cancer development.

205
Q

Summarize the activities of the 2 APC complexes in mitosis and G1:

A

•APC/C Cdc20

206
Q

True or false?

207
Q

•S phase initiation requires an ordered sequence of events starting right after completion of mitosis:

A

-anaphase/early G1(low Cdk activity due to APCCdh1)

208
Q

Pre Rc only forms when there is _________ cdk activity, which is only found in ______ as a result of APC/C _________

209
Q

At S and on there is high cdk activity occurs, preventing formation of another pre RC. True or false?

210
Q

Get info from slide 59 of 17/18

211
Q

In regards to replication, what happens in G1?

A

G1 pre-RC assembly (licensing)

212
Q

In regards to replication, what happens in S? (3)

A

S phase- Initiation of replication

213
Q

In terms of replication, what happens in G2/M?

A

G2/M- Prevention of re-replication

214
Q

In terms of replication, what happens in anaphase?

A

Anaphase- re-creating conditions for pre-RC formation (licensing)

215
Q

Describe what happens in terms of preRC formation, then inactivation of its components, then how they are eventually promoted again:

A

pre-RC: ORC recruits Cdc6 and Cdt1 which recruit Mcm helicase.

216
Q

Summarize main events and main activities of the cell cycle:

A

•G1- low Cdk activity. PreRCs assemble.

217
Q

What are cell cycle checkpoints?

A

•Delay or arrest in cell cycle progression in response to problems completing a specific step in the cell cycle or in response to other cellular problems

218
Q

How do checkpoints take action? (3)

A

•Checkpoints may pause the cell cycle and promote repair before continuing. Checkpoints can also induce permanent arrest or apoptosis.

219
Q

True or false?

220
Q

What are the important checkpoints? (3)

A
  1. Spindle assembly checkpoint
221
Q

Describe what the spindle assembly checkpoint is and the way it takes place:

A

•APC/Cdc20 is inhibited in response to incomplete kinetochore/microtubule attachments.

222
Q

Briefly describe G1 DNA damage checkpoint and its significance:

A

•activated if DNA damage is detected in G1 –> G1 arrest.

223
Q

Briefly describe replicative senescence and its significance:

A

•Replicative senescence - telomere shortening –> G0 arrest (senescence).

224
Q

What are the three situations that trigger the DNA damage checkpoint?

A
  1. Stalled replication fork
225
Q

What do the 3 DNA damage triggers result in?

A

They recruit ATR and ATM, 2 kinases that phosphorylate 2 downstream kinases (chk1 and chk2).

226
Q

What are ATR and ATM responsible for (aside from chk1 and chk2 phosphorylation)?

A

ATM - double strand breaks (leads to permanent cell-cycle arrest or cell death)

227
Q

What do chk1 and chk2 do?

A

Chk1: production of DNA repair enzymes

228
Q

ATM (and ATR) has two functions at these sites:

A
  1. help recruit repair machinery
229
Q

What did they do to cells to show ATM recruitment?

A

hit em with ionizing radiation

230
Q

Read over well

231
Q

Wee1 and cdc25 act on what?

A

cdk1 and cdk2

232
Q

Get info from slide 9 of lecture 19

233
Q

Provide the G1 DNA damage checkpoint pathway:

A

•ATR and ATM both recognize different types of DNA damage.

234
Q

A very similar checkpoint to DNA damage in g1 can be activated in G2:

A

•Cdk1 remains phosphorylated by Wee1

235
Q

•In case of more severe damage ATM,ATR, Chk1 and Chk2 phosphorylate and activate what?

236
Q

Describe p53 activity:

A

•p53 is a transcription factor that induces a permanent cell cycle arrest by activating p21 expression

237
Q

Explain how p53 mediates G1 arrest in response to DNA damage:

A

In undamaged cells p53 is inactive due to Mdm2 binding

238
Q

Briefly indicate how telomeres are protected and what they are protected from:

A

•Telomeres Are Protected by telomere binding proteins - sheltrin complex

239
Q

Describe replicative senescence pathway:

A

•Telomere shortening at each cell division eventually leads to loss of all of the telomere repeats.

240
Q

Why is p53 considered the cellular gatekeeper?

A

because many issues like DNA damage, telomere shortening and hypoxia lead to its activation, resulting in cell cycle arrest, senescence, or apoptosis

241
Q

What is apoptosis and briefly how does it get triggered?

A

•Apoptosis is often referred to as programmed cell death or cell suicide.

242
Q

What are these?

A

Examples of apoptosis as a developmental process

243
Q

•Apoptosis as a response to cell cycle and other cellular checkpoints. True or false?

244
Q

What are the big advantages of using c. elegans for apoptosis?

A

One of the big advantages in c.elegans is that it has a very limited number of cells and because it is see-through, you can follow every single cell during development

245
Q

What information did they get from c. elegans on apoptosis?

A

Showed that programmed cell death was revealed through cell lineage maps

246
Q

Explain the difference between apoptosis and necrosis:

A

•Apoptosis involves activation of a cell death pathway while necrosis is a passive process resulting from damage to the cell.

247
Q

•Features of apoptotic cells: (things that happen)

A

-cytoskeleton collapse, nuclear envelope breaks down, chromatin condenses and breaks into fragments, cell surface blebbing, apoptotic bodies

248
Q

Apoptotic cells identified by incubation in Acridine Orange between digits of hands. Describe how this can be determined experimentally:

A

Incubating with dna dye called acridine orange binds to dna regardless of alive or dead. But, it cannot enter the membrane of a living cell. The cell membrane loses its integrity in apoptosis, so it allows for acridine orange to enter, so it specifically shows where apoptotic cells are.

249
Q

What would you see on a DNA gel in apoptotic cell?

A

Chromosomal DNA fragmentation detected on a DNA gel (fragmentation as time goes on)

250
Q

Describe TUNEL labelling:

A

TUNEL labeling - apoptotic cells have fragmented chromosomes. Label DNA ends with Terminal deoxynucleotidyl Transferase

251
Q

Name and describe the 5 assays for apoptosis:

A

•Plasma membrane loses integrity

252
Q

What is the state of caspases during normal times in the cell?

A

Caspases are in our cells at all times in a state in which they need the n terminus to be cleaved to be active (procaspase to caspase)

253
Q

get slide 9 of lecture 20 info

254
Q

True or false?

255
Q

Two classes of caspase:

A

•Initiator (activator) caspases - cleave other caspases

256
Q

True or false?

257
Q

What are the 2 pathways for activation of caspases?

A

Intrinsic and extrinsic pathway

258
Q

Briefly explain the intrinsic pathway:

A

-cellular response to various stresses, DNA damage, depletion of survival factors.

259
Q

Briefly explain the extrinsic pathway:

A

-apoptosis induced via signal from specialized cells - eg cytotoxic T-lymphocytes

260
Q

What does this describe?

A

Intrinsic pathway

261
Q

What is the intrinsic pathway of apoptosis promoted by? Explain.

A

•regulated by BH-Domain family of proteins

262
Q

True or false?

263
Q

3 important categories of BH-domain proteins. Name and briefly indicate the role of each:

A

BH123 - forms the mitochondrial pore which releases cytochrome c (and anti-IAPs)

264
Q

Bh3-only are pro-apoptotic because they bind to and inhibit ___________, allowing for ___________ pore formation in mitochondrial membrane

265
Q

Read over well

266
Q

Cytochrome C release from the mitochondria is a key event in the ___________ pathway.

267
Q

Explain what happens once cytochrome C is released from the mitochondria:

A

Cytochrome C release - binding to Apaf1 –> CARD domain exposed - multimerization (Apoptosome)

268
Q

•________________ activated by cleavage - cleaves ________________ caspases.

269
Q

What are IAPs?

A

IAPs are inhibitors of apoptosis, they sit around and are ready to bind to any activated caspase to block it. They can block apoptosis even if initiated properly.

270
Q

What are anti-IAPs? Give an example of one and describe what they do:

271
Q

What does this describe?

272
Q

What does this describe?

273
Q

Summarize the Intrinsic Pathway of Apoptosis

A

•aggregation of BH123 proteins - make a pore in mitochondria

274
Q

Describe the regulation of the intrinsic pathway:

A

•survival factors (anti-apoptotic)

275
Q

add info from slide 28 of lecture 20

276
Q

add info from slide 29 of lecture 20

277
Q

Describe how cell competition leads to apoptosis:

A

•Cell competition leads to apoptosis. Major mechanism for organizing neural connections.

278
Q

Describe how growth factors can be survival factors:

A

A growth factor/survival factor binds to a receptor, stimulating a pathway in which Akt kinase is activated, which can phosphorylate Bad (BH3-only protein) to allow for active Bcl2. This Bcl2 can go on to block apoptosis by preventing BH123 aggregation and mitochondrial pore formation

279
Q

Describe how mitogens can be survival factors:

A

Mitogen binds to activate a receptor that stimulates a pathway that activates MAPK, which can phosphorylate Hid (anti-IAP) to inactivate it, allowing for IAPs to be free to block apoptosis by binding to caspase

280
Q

is p53 anti or pro apoptotic?

A

pro-apoptotic

281
Q

get info from slide 35 lecture 20

282
Q

get info from slide 36 lecture 20

283
Q

What are the 5 ways that p53 works as a pro-apoptotic transcription factor?

A

p53 induces BH3-only expression

284
Q

Read over very well

285
Q

What mediates extrinsic apoptosis?

A

Cytotoxic T-cells binding to virus-infected cells

286
Q

Describe the recognition of virus-infected cells:

A

MHC proteins + peptide on cell surface

287
Q

True or false?

288
Q

True or false?

289
Q

get slide 46 info from lec 20

290
Q

What is Fas-mediated Extrinsic Apoptosis?

A

•FasL - a ligand of the Tumour Necrosis Factor (TNF) family of proteins - integral membrane protein ligands - function as homotrimers.

291
Q

p53 is primary inducer of intrinsic pathway, but also promotes extrinsic by promoting fas receptor expression. true or false?

292
Q

get missing info from slide 48 of lec 20

293
Q

Summarize all that happens in apoptosis mediated by CTLs (cytotoxic T-lymphocytes)

A

•Cytotoxic T cells identify infected cells via T cell receptor binding to foreign peptides presented on MHC receptors.

294
Q

-____________ tumour - cancer that spreads to ____________ sites - via travel of cancer cells through ____________ or ____________ system.

295
Q

What are carcinomas, sarcomas, leukemias, and lymphomas?

A

•Carcinomas - arise from epithelial cells - most common and most dangerous cancers in humans.

296
Q

True or false?

297
Q

What are the original theories on the origins of cancer? (2)

A

•Chemicals and other agents that damage DNA (mutagens) as causes of cancer

298
Q

Read over very well

299
Q

Indicate some phenomena we see in normal cells growing in culture (4)

A

Cells grown in culture form a monolayer:

300
Q

•Chemicals and radiation can transform normal cells into cancer cells in vitro. What are the 4 traits that suggest that they have become cancer cells?

A

•loss of contact inhibition

301
Q

These 4 traits that indicate cancer cells led to what conclusion?

A

•These agents cause mutations –> cancer is caused by mutations in our genes

302
Q

Indicate the significance of Rous sarcoma virus (RSV):

A

First characterized tumour virus. Led to model that cancer is caused by infectious agents.

303
Q

Describe the experiment done with RSV and why they did it:

A
  • removed sarcoma from chicken and broke up into small tissue chunks
304
Q

1960’s - Infection with RSV leads to: (4)

A

•loss of contact inhibition

305
Q

What kind of virus is RSV?

A

Retrovirus –> rna genome, carry reverse transcriptase to make DNA copy, which is integrated into genome

306
Q

Just read

307
Q

In 1974, they discovered how RSV was able to transform normal cells to cancerous. Briefly state what this was:

A

a single viral gene - src

308
Q

RSV contains the Src gene - and this gene is the one that confers transformation ability to cells. True or false?

309
Q

Just read

310
Q

What were the problems with the viral theory for cancer?

A
  1. They had trouble finding the viruses that caused these human cancers
311
Q

True or false?

312
Q

What did they later realize about src?

A

They realized that they all contain src gene whether infected or not, and it looks like a normal euk gene (introns, exons), whereas the viral src gene doesn’t have those introns

313
Q

True or false?

314
Q

So, what did they conclude about the src gene in RSV?

A

transforming gene from RSV is a gene that originated in the host (chicken) and got incorporated into the virus at some point. This gene gave the virus a selective advantage and was therefore retained in the viral genome.

315
Q

Ultimately, the understanding of the src gene led to the unification of the viral and genetic origin of cancer theories. Explain:

A

•Cancer is caused by overexpression of specific genes that originated from our own genome (proto-oncogenes), that are carried in viruses (viral oncogenes).

316
Q

What are these viral oncogenes usually involved in?

A

A lot of these viral oncogenes are genes that play important roles in growth and cell division.

317
Q

Slow acting vs fast acting tumour viruses: (I don’t really understand this concept)

A

•slower acting tumour viruses may act by inserting near and causing high level expression of host oncogenes. This would only occur by chance after many rounds of cell infection.

318
Q

Slower acting because it requires chance event of landing in the right place for greater expression (Enhancers). True or false?

319
Q

What did these discoveries about viral oncogenes suggest about chemical mutagens? How can you prove this?

A

• Suggested the idea that chemical mutagens cause cancer by converting proto-oncogenes into oncogenes

320
Q

Describe transfection:

A

Transfection:

321
Q

true or false?

322
Q

Explain how transfection can cause cancer in mice from human tumour cells?

A

•transfect normal mouse cells with DNA from a human tumour

323
Q

How were they able to identify the actual altered gene that caused the transformation of the cells?

A

•genomic DNA library from these transformed mouse cells

324
Q

True or false?

325
Q

Read over well

326
Q

What mutation in the Ras gene could have made it constitutively active?

A

Mutation in GTPase activity that makes it stuck in GTP bound state

327
Q

Name and describe the 4 ways proto-oncogenes can be converted to oncogene:

A
  1. Deletion or point mutation in coding sequence –> hyperactive protein made in normal amounts
328
Q

What can be used to identify cancer as a result of chromosomal rearrangement?

A

SKY probe that labels diff colours for diff chromosomes

329
Q

Forms of activation of oncogenes in cancer (5)

A

•viral copy of oncogene expressed at high levels by viral enhancers.

330
Q

Describe the experiments and subsequent interpretation of them that led to the discovery of tumour suppressor genes:

A

•Cell fusion experiments: Fuse a cancer cell with a normal cell

331
Q

Describe the 2 forms of retinoblastoma:

A

Familial and sporadic

332
Q

This led to the idea of the tumour suppressor and what hypothesis?

A

two-hit hypothesis

333
Q

get explanation of slide 36 (lec 21)

334
Q

Besides genetic changes, how else could loss of heterozygosity occur?

A

•Loss of heterozygosity can also occur by epigenetic gene silencing - somatically inherited chromatin modifications

335
Q

What are Rb and INK4 considered? Why?

A

tumour suppressors

336
Q

What is the most important tumour suppressor?

337
Q

Go through slide 39 chart of what happens as a result of p53 mutation

A

green - breast cancer

338
Q

•Rb identified as the first tumour suppressor gene. True or false?

339
Q

What are most familial cancers caused by?

A

•Most familial cancers are caused by inheritance of recessive mutant alleles of tumour suppressor genes.

340
Q

Why elephants rarely get cancer

A

•elephants live almost as long as humans - up to 70 years

341
Q

What does this mean?

A

Cancer requires oncogenes and mutant tumour suppressors

342
Q

Explain Clonal Origins of Cancer:

A

•Most cancers derive from a single cell that acquires a somatic mutation that helps promote tumour formation.

343
Q

Just read over well

344
Q

Get info from slide 48 (lecture 21)

345
Q

When can genomic rearrangements occur?

A

As a result of genome instability:

346
Q

Explain genome instability:

A

•chromosome rearrangements, gene amplification, anneuploidy

347
Q

cancer results from accumulation of mutations that give the cell the following capabilities: (7)

A

•Self sufficiency in growth signals and/or insensitivity to anti-growth signals - eg.. ras activation, Rb loss

348
Q

Is the order of acquiring these capabilities important? Explain:

A

No. The order of acquiring these capabilities is not important but once genome instability is acquired, other mutations arise faster

Metabolism (14 decks)

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