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MolCell Mega Class > PRIVETTE-VINNEDGE 3 > Flashcards

PRIVETTE-VINNEDGE 3 Flashcards

1
Q

What is the main purpose of the G2 phase?

A

The G2 phase ensures the DNA is replicated and undamaged before the cell enters mitosis.

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2
Q

How long does the G2 phase typically last?

A

The G2 phase is relatively short, taking only about 4 hours to complete.

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3
Q

What happens if DNA damage, particularly double-strand breaks, is detected during G2?

A

Homologous recombination DNA repair is activated, using the sister chromatid created during S phase as a template.

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4
Q

Which kinases are involved in mediating homologous recombination repair?

A

ATM/ATR kinases mediate HR repair.

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5
Q

What is the consequence of checkpoint activation in response to DNA damage?

A

Checkpoint activation inhibits the M phase cyclin-CDK complex (Cyclin B/CDK1), preventing entry into mitosis until the damage is repaired.

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6
Q

What triggers the transition from G2 to M phase?

A

An inactive DNA damage checkpoint signals that the DNA is intact and replication is complete, allowing the cell to proceed to mitosis.

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7
Q

Besides DNA repair, what other important processes occur during the G2 phase?

A

The cell accumulates essential proteins required for mitosis, including mitotic checkpoint proteins, mitotic spindle proteins (tubulins), and cytokinesis proteins.

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8
Q

What are centrosomes composed of?

A

Each centrosome consists of two centrioles.

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9
Q

When are centrosomes duplicated?

A

Centrosomes are duplicated during the S phase, initiated by cyclin E/CDK2.

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10
Q

When do centrosomes elongate and mature?

A

Centrosomes elongate and mature during the G2 phase.

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11
Q

What happens to the centrosomes during the M phase?

A

The duplicated centrosomes are separated and move to opposite poles of the cell during the M phase.

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12
Q

What is the master regulator of centrosome duplication?

A

PLK4 kinase plays a crucial role in regulating centrosome duplication.

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13
Q

What is another name for centrosomes?

A

Centrosomes are also known as microtubule-organizing centers (MTOCs).

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14
Q

What is the primary function of centrosomes?

A

Centrosomes serve as the origin for microtubule nucleation and mitotic spindle pole formation.

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15
Q

What protein serves as a marker for centrosomes?

A

Gamma (γ) tubulin is a specific marker for centrosomes.

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16
Q

Which kinases are essential for centrosome maturation, separation, and movement to opposite poles of the cell?

A

Aurora kinase and Polo-like kinase 1 (PLK1) are critical for these centrosome-related processes.

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17
Q

How do centrosomes move towards the poles of the cell?

A

They recruit KIF11, a microtubule-dependent motor kinesin-like protein, which pushes them towards the poles.

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18
Q

What are the two main mitotic checkpoints?

A

The two main mitotic checkpoints are the Antephase (Prophase) Checkpoint and the Metaphase Checkpoint.

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19
Q

What does the Antephase (Prophase) Checkpoint monitor?

A

It checks if the mitotic spindle can develop properly by assessing microtubule polymerization and stability during prophase.

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20
Q

How is the activation of the Antephase Checkpoint assessed?

A

It’s assessed by comparing the percentage of cells in prophase versus other cell cycle stages.

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21
Q

What is the primary focus of the Metaphase Checkpoint?

A

This checkpoint determines if all sister chromatids are attached to the mitotic spindle and correctly aligned at the metaphase plate.

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22
Q

What molecular complex drives the Metaphase Checkpoint?

A

The mitotic checkpoint complex (MCC), composed of BubR1, Bub3, Mad2, and Cdc20, is responsible for this checkpoint.

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23
Q

How does the MCC exert its control at the Metaphase Checkpoint?

A

The MCC inhibits the Anaphase Promoting Complex (APC/C), preventing the separation of sister chromatids until proper attachment is ensured.

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24
Q

What holds sister chromatids together until the Metaphase Checkpoint is satisfied?

A

The Cohesin complex maintains the connection between sister chromatids.

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25
Q

What factors can activate the Prophase/Antephase checkpoint?

A

This checkpoint can be triggered by cold temperatures and microtubule-targeting drugs like paclitaxel and nocodazole.

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26
Q

What is the key mediator of the Prophase/Antephase checkpoint?

A

CHFR, an E3 ubiquitin ligase, plays a crucial role in this checkpoint.

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27
Q

What is the full name of CHFR?

A

CHFR stands for Checkpoint with Forkhead-associated and RING finger domains.

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28
Q

How does microtubule instability affect CHFR?

A

Microtubule instability leads to the stabilization of CHFR.

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29
Q

What is the function of CHFR in the checkpoint?

A

CHFR ubiquitinates PLK1, targeting it for degradation. This allows Wee1 kinase to inhibit CDK1, halting the cell cycle.

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30
Q

What other kinase can activate this checkpoint pathway?

A

p38 MAPK kinase, a stress sensor, can also activate the Prophase/Antephase checkpoint pathway.

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31
Q

Where are checkpoint proteins located during metaphase?

A

They are localized to the kinetochore.

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32
Q

What is the kinetochore?

A

It is the centromere region of the chromosome where the spindle microtubules attach.

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33
Q

What is the role of CENP-E in metaphase?

A

CENP-E, a centromeric kinesin motor protein, binds to unattached kinetochores and pulls them towards the microtubule spindles.

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34
Q

What happens when CENP-E binds to microtubules?

A

CENP-E releases Aurora kinases, which triggers the transition into anaphase.

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35
Q

What activates the metaphase checkpoint?

A

The checkpoint is activated by the absence of tubulins or tension at the kinetochore, indicating improper attachment of chromosomes to the spindle.

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36
Q

What happens to CENP-E when it is not attached to microtubules?

A

It restricts Aurora kinases and activates BUB1.

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37
Q

What are the roles of BUB1 and MPS1?

A

Both BUB1 and MPS1 are kinases.

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38
Q

How does MAD2 function in the metaphase checkpoint?

A

MAD2 undergoes a conformational change upon kinetochore attachment to spindle tubulins, contributing to checkpoint signaling.

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39
Q

What is the consequence of activating the metaphase checkpoint?

A

Activation of this checkpoint blocks the Anaphase Promoting Complex (APC/C), preventing the cell from progressing to anaphase.

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40
Q

What is a common consequence of the loss of mitotic checkpoints?

A

Loss of mitotic checkpoints frequently occurs in cancer.

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41
Q

Why are CHFR and other checkpoint proteins considered tumor suppressors?

A

They prevent uncontrolled cell division by ensuring proper chromosome segregation. Defects in these proteins can contribute to tumor development.

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42
Q

What happens when mitotic checkpoints are defective?

A

Mitosis can occur even if the mitotic spindle and sister chromatids are not properly connected, leading to errors in chromosome segregation.

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43
Q

What is the result of improper chromosome segregation into daughter cells?

A

It results in chromosome instability (CIN), leading to aneuploidy.

44
Q

How can chromosome instability (CIN) be detected?

A

CIN can be detected by observing lagging or misaligned chromosomes, micronuclei by immunofluorescence, and DNA content greater than 4N by flow cytometry.

45
Q

What is aneuploidy?

A

Aneuploidy refers to having an abnormal number of chromosomes in a cell.

46
Q

What problems can arise from having more centrosomes than normal?

A

Excessive centrosomes can lead to the formation of multipolar spindles, contributing to chromosome missegregation and aneuploidy.

47
Q

Describe the state of chromatin during interphase.

A

Interphase chromatin is already compacted but requires further condensation during mitosis.

48
Q

What mediates chromatin condensation during mitosis?

A

Condensation is mediated by Condensin I and II complexes and histone modifications.

49
Q

How is chromosome looping accomplished during condensation?

A

Condensins facilitate chromosome looping through a loop exclusion process.

50
Q

What defines the boundaries of chromosome loops?

A

CTCF protein binding sites mark the boundaries of chromosome loops.

51
Q

What type of motor protein is believed to be involved in chromatin condensation?

A

Evidence suggests that a chromatin kinesin motor protein, possibly KIF4, is required for this process.

52
Q

What are topologically associating domains (TADs)?

A

TADs are folded chromatin loops that span hundreds of kilobases, contributing to the three-dimensional organization of the genome.

53
Q

What techniques can be used to identify the long-range cis-interactions that form TAD structures?

A

Techniques based on proximity-ligation and sequencing, such as Hi-C, can be used to map these interactions genome-wide.

54
Q

What are the two main processes involved in chromatin condensation?

A

Condensation involves loop formation by condensins and histone H3 and H4 modifications.

55
Q

How does PLK1 contribute to histone modifications during condensation?

A

PLK1 activates Haspin, which phosphorylates histone H3 at threonine 3 (T3).

56
Q

What is the role of Aurora B kinase in histone modifications?

A

Aurora B kinase phosphorylates histone H3 at serine 10 (S10) and serine 28 (S28).

57
Q

What is the line in the middle of metaphase called?

A

The metaphase plate

58
Q

The midbody is based on _______ and ________.

A

actin, septins

59
Q

The ______ spindles of the microtubules point away from the cell.

A

astral

60
Q

__________ microtubules are microtubules that connect to each other and act as the pulling force.

A

Interpolar

61
Q

What happens to histone H4 during condensation?

A

Histone H4 undergoes deacetylation at lysine 16 (K16) by Hst2p.

62
Q

The Antephase (Prophase) Checkpoint is for the _______, while the Metaphase Checkpoint was discovered first and is for checking that the spindles are attached to every ________.

A

microtubules, sister chromatid

63
Q

How is histone H3 methylation reversed after mitosis?

A

PP1 phosphatase reverses histone H3 methylation.

64
Q

What is cytokinesis?

A

Cytokinesis is the final stage of the cell cycle, where a single cell divides into two daughter cells.

65
Q

True or False: Extra centrosomes are always bad and will cause errors.

A

True, conserved across species and cell types

66
Q

What events occur during telophase and cytokinesis?

A

The nuclear envelope reassembles, and a contractile ring forms, leading to the division of the cytoplasm.

67
Q

What forms the contractile ring during cytokinesis?

A

The contractile ring is made of actin filaments and myosin.

68
Q

What is the cleavage furrow?

A

The cleavage furrow is the indentation that forms in the cell membrane as the contractile ring pinches the cytoplasm.

69
Q

What is abscission?

A

Abscission is the final separation of the two daughter cells.

70
Q

What is the role of PRC1 in cytokinesis?

A

PRC1 (Protein Regulation of Cytokinesis 1), a microtubule-associated protein, helps regulate the process of cytokinesis.

71
Q

What is the function of the Chromosomal Passenger Complex (CPC)?

A

The CPC plays a key role in controlling chromosome segregation and cytokinesis.

72
Q

How does Rho-associated Kinase (ROCK) contribute to cytokinesis?

A

ROCK is involved in regulating the assembly and contraction of the contractile ring.

73
Q

What is the role of ECT2 in cytokinesis?

A

ECT2 is a Rho-GEF that activates Rho GTPases, which are essential for contractile ring formation.

74
Q

What is the function of the Central Spindle Complex (CSC2/Borealin)?

A

The Central Spindle Complex helps organize the microtubules in the central spindle, which is crucial for cytokinesis.

75
Q

What is the function of Myosin II motor proteins during cytokinesis?

A

Myosin II motor proteins drive the contraction of the central ring at the cleavage furrow, leading to cell separation.

76
Q

What is the role of the Endosomal Sorting Complex Required for Transport (ESCRT) in cytokinesis?

A

The ESCRT complex is part of the abscission machinery, responsible for the final cutting of the membrane connection between daughter cells.

77
Q

What are septins (SEPT)?

A

Septins are cytoskeletal scaffolding proteins that play important roles in cytokinesis.

78
Q

How do septins contribute to cytokinesis?

A

They interact with anillin and myosin, facilitating the shrinkage of the cleavage furrow into the midbody.

79
Q

What is the midbody?

A

The midbody is a transient structure that forms between the two daughter cells during cytokinesis, containing remnants of the spindle microtubules and other proteins.

80
Q

How do septins facilitate abscission?

A

They help activate the ESCRT complex, which is required for the final membrane separation.

81
Q

What other role do some septin proteins have in cell division?

A

Some septins bind to the kinetochore and facilitate chromosome alignment at the metaphase plate.

82
Q

How do septins help develop the cytokinetic bridge/midbody?

A

They stabilize the structure of the cytokinetic bridge.

83
Q

What structure do anillin and septins create during cytokinesis?

A

They form a “collar” that flanks the midbody.

84
Q

What is the purpose of the “collar” formed by anillin and septins?

A

It helps recruit and localize the ESCRT-III complex, which is essential for abscission.

85
Q

What can result from incorrect cytokinesis or multipolar spindles?

A

Errors in cytokinesis can lead to the formation of binucleated cells, which are single large cells with two or more nuclei.

86
Q

What typically happens to normal binucleated cells?

A

Most normal binucleated cells either get stuck in the next G1 phase or undergo apoptosis.

87
Q

In what type of cells are multinucleated cells considered normal?

A

Normal multinucleated cells are rare but are primarily observed in cardiomyocytes, the muscle cells of the heart.

88
Q

Why are binucleated cells commonly seen in cancer?

A

Cancer-associated mutations can enable binucleated cells to continue proliferating.

89
Q

What are the consequences of binucleated cells continuing to proliferate in cancer?

A

This can be a significant driver of aneuploidy and mutagenesis, contributing to tumor development and progression.

90
Q

Why is the cell cycle a target for cancer therapy?

A

Cancer cells often exhibit uncontrolled cell cycle progression. Targeting cell cycle checkpoints and processes can inhibit their proliferation.

91
Q

What types of drugs target the cell cycle in cancer treatment?

A

Examples include microtubule-targeting drugs (e.g., taxanes), CDK inhibitors, and DNA damaging agents.

92
Q

What are the four main phases of the cell cycle?

A

The cell cycle consists of G1, S, G2, and M phases.

93
Q

What is the role of cyclins and CDKs in the cell cycle?

A

Cyclins and cyclin-dependent kinases (CDKs) are regulatory proteins that control the progression through the cell cycle.

94
Q

What are cell cycle checkpoints?

A

Checkpoints are control mechanisms that ensure the proper order and completion of cell cycle events and prevent errors in DNA replication and chromosome segregation.

95
Q

What is the significance of chromosome instability (CIN) in cancer?

A

CIN is a hallmark of cancer and contributes to tumor heterogeneity, drug resistance, and metastasis.

96
Q

What are some consequences of errors in mitosis?

A

Errors in mitosis can lead to aneuploidy, chromosome rearrangements, and cell death.

97
Q

How does the cell cycle relate to tissue development and repair?

A

The cell cycle is essential for cell proliferation, which is crucial for tissue growth, development, and repair.

98
Q

What is the role of apoptosis in maintaining tissue homeostasis?

A

Apoptosis, or programmed cell death, eliminates damaged or unwanted cells, preventing the accumulation of mutations and maintaining tissue health.

99
Q

What is the difference between mitosis and meiosis?

A

Mitosis produces two identical daughter cells, while meiosis produces four genetically diverse daughter cells involved in sexual reproduction.

100
Q

How does the cell cycle contribute to aging?

A

With each cell division, telomeres shorten, eventually leading to cellular senescence and contributing to the aging process.

101
Q

True or False: The G2 phase is longer than the S phase.

A

False. The G2 phase is typically shorter than the S phase.

102
Q

True or False: Centrosomes are only present during mitosis.

A

False. Centrosomes are present throughout the cell cycle but play a critical role in organizing the mitotic spindle during mitosis.

103
Q

True or False: Activation of mitotic checkpoints promotes cell cycle progression.

A

False. Checkpoint activation halts or delays the cell cycle until specific conditions are met, ensuring the fidelity of cell division.

104
Q

True or False: Cytokinesis occurs before mitosis.

A

False. Cytokinesis is the final stage of the cell cycle, following mitosis.

105
Q

True or False: Errors in the cell cycle can contribute to the development of cancer.

A

True. Uncontrolled cell division and errors in DNA replication or chromosome segregation can lead to the accumulation of mutations and the development of cancer.

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