Chapter 18 - The Cell Division Cycle Flashcards

1
Q

The entire period between one M phase and the subsequent M phase is called what?

  • anaphase
  • prophase
  • metaphase
  • interphase
  • G1 phase
A

Interphase

Correct; interphase consists of S phase plus the two gap phases, G1 and G2.

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2
Q

What must happen for a Cdk to be active?

  • It must translocate from the cytoplasm to the nucleus.
  • It must bind to its cyclin partner.
  • It must increase in concentration at a specific time in the cycle.
  • It must be switched on by proteolysis.
  • It must dissociate from its bound cyclin.
A

It must bind to its cyclin partner

(A Cdk must bind its cyclin before it can become enzymatically active. A Cdk unbound to a cyclin does not retain kinase activity.)

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3
Q

The inactivation of M-Cdk leads to which of the following?

  • exit from mitosis
  • exit from S phase
  • onset of mitosis
  • onset of G2 phase
  • onset of S phase
A

Exit from mitosis

(The degradation of M cyclin and inactivation of M-Cdk lead to the molecular events that take the cell out of mitosis and into interphase.)

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4
Q

The cell-cycle control system initiates chromosome segregation only after which of the following has occurred?

  • The cell stops growing.
  • DNA has been completely replicated and the chromosomes have decondensed.
  • Cytokinesis is complete.
  • The duplicated chromosomes are correctly aligned on the mitotic spindle.
  • M phase is complete.
A

The duplicated chromosomes are correctly aligned on the mitotic spindle.

(Chromosome segregation takes place after the duplicated chromosomes are correctly attached to kinetochore proteins that interact with the microtubules of the mitotic spindle.)

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5
Q

What do cells do during G1 phase?
Choose one or more:

  • replicate DNA
  • separate sister chromatids
  • repair DNA damage
  • destroy cyclins
A
  • Repair DNA damage
  • Destroy cyclins

(During G1, cells grow and monitor the environment before committing to a new round of cell division. They can delay further progression through the cycle to repair damaged DNA. All Cdks are inactivated during G1, by cyclin degradation, to prevent an early entry into the cell cycle.)

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6
Q

Most of the diversity in the rates of cell division in the adult body lies in variations in the time that each cell spends in which phase(s)?

  • S phase and M phase
  • G1 phase and G2 phase
  • S phase
  • M phase
  • G1 phase and G0 phase
A

G1 phase and G0 phase

Cells that divide every year or two spend the vast majority of that time—all but 12 to 24 hours—in G0 and G1.

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7
Q

The signal to commence DNA replication comes from which of the following?

  • S-Cdk
  • the destruction of M-Cdk
  • ORC
  • the destruction of Cdc6
A

S-Cdk

(S-Cdk, assembled and activated at the end of G1, initiates DNA replication by activation of the DNA helicases in the prereplicative complex, promoting the assembly of the proteins that form the replication fork.)

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8
Q

If DNA is damaged or incompletely replicated in S phase, the inhibition of which of these molecules prevents the cell from entering M phase?

  • p53
  • S-Cdk
  • Cdc6
  • Cdc25
  • ORC
A

Cdc25

(For M-Cdk to be activated, the phosphatase Cdc25 must remove inhibitory phosphates from M-Cdk; inhibition of this activity can delay entry into M phase.)

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9
Q

In most respects, cell division is similar between plant and animal cells. Which of the following events occurs by a different mechanism in animal and plant cells?

  • separation of sister chromatids
  • condensation of chromosomes at the beginning of cell division
  • separation of the cell into two daughter cells
  • chromosomes being pulled apart by the microtubules of the mitotic spindle
  • alignment of chromosomes in the center of the cell
A

Separation of the cell into two daughter cells

Cytokinesis, the separation of the cell into two new daughter cells, occurs differently in plant and animal cells.

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10
Q

True or False

Chromosomes condense and move to the center of the cell before sister chromatids separate in anaphase.

A

True

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11
Q

The chromosomes decondense in _______ before cytokinesis is complete.

A

telophase

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12
Q

What is the mitotic spindle made of?

  • microtubules
  • cohesins
  • condensins
  • actin and myosin
A

Microtubules

(The complete mitotic spindle is composed of these microtubules along with the various proteins that interact with them.)

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13
Q

Why does the activation of M-Cdk begin abruptly?

  • M cyclin increases abruptly.
  • The mitotic Cdk increases abruptly.
  • Each M-Cdk complex can activate more M-Cdk.
  • M cyclin is rapidly phosphorylated and thereby activated.
A

Each M-Cdk complex can activate more M-Cdk.

(The abrupt activation of M-Cdk depends on the removal of inhibitory phosphates by Cdc25; activated M-Cdk activates more Cdc25, thus promoting activation of additional M-Cdk through a positive feedback loop.)

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14
Q

The mitotic spindle begins to assemble in which phase of the cell cycle?

  • telophase
  • prometaphase
  • prophase
  • anaphase
  • metaphase
A

Prophase

The mitotic spindle begins to assemble during the initial stage of mitosis once interphase has completed.

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15
Q

Microtubules capture chromosomes by binding specifically to which of the following?

  • kinetochores on the sister chromatids
  • telomeres on the condensed chromosomes
  • condensins on the condensed chromosomes
  • cohesins on the sister chromatids
A

Kinetochores on the sister chromatids

(Microtubules capture chromosomes by binding to kinetochores on the sister chromatids. Kinetochore proteins assemble at the centromere of each condensed chromosome.)

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16
Q

Which of the following occurs during metaphase?

  • chromosomes being aligned under tension at the spindle equator
  • nuclear envelope reassembly
  • nuclear envelope breakdown
  • chromosomes being captured by spindle microtubules
  • chromosomes being condensed
A

Chromosomes being aligned under tension at the spindle equator

(During metaphase, chromosomes are aligned under tension at the spindle equator.)

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17
Q

What is the contractile ring made of?

  • integrins
  • cohesins
  • microtubules
  • actin and myosin
  • condensins
A

Actin and myosin

(The sliding of actin filaments against myosin proteins generates the force needed to pinch off the plasma membrane and form two cells.)

18
Q

In dividing plant cells, a new cell wall is formed between two sets of chromosomes via a structure called a phragmoplast, which is built by vesicles largely originating from which organelle?

  • vacuole
  • endoplasmic reticulum
  • vesicles from the broken-down nuclear envelope
  • Golgi apparatus
  • chloroplast
A

Golgi apparatus

(Correct; these membrane-enclosed vesicles fuse to form a disclike, membrane-enclosed structure that expands until it reaches the plasma membrane and original cell wall.)

19
Q

When a cell is acutely injured, it usually dies by which process?

  • apoptosis
  • endocytosis
  • phagocytosis
  • necrosis
A

Necrosis

Necrotic cells typically swell and burst, causing local inflammation.

20
Q

Which of the following statements is false?

  • Some death-inhibiting members of the Bcl2 family inhibit apoptosis by blocking cytochrome c release from mitochondria.
  • Bax and Bak are death-promoting members of the Bcl2 family that induce the release of cytochrome c from mitochondria into the cytosol.
  • Some Bcl2 family members promote apoptosis, whereas others inhibit apoptosis.
  • The death-promoting members of the Bcl2 family include Bcl2 itself.
A

The death-promoting members of the Bcl2 family include Bcl2 itself.

(Bcl2 inhibits apoptosis. Thus, it cannot be considered to be death-promoting.)

21
Q

Which of the following statements describes how growth factors stimulate animal cell enlargement?

  • They stimulate microtubule polymerization.
  • They stimulate protein degradation.
  • They stimulate intracellular protein synthesis.
  • They stimulate an influx of extracellular water into the cytosol.
A

They stimulate intracellular protein synthesis.

Growth factors increase the rate of protein synthesis and decrease the rate of protein degradation.

22
Q

What are example of active Cdk?

A
  • Cdk bound to cyclin
  • Threonine in T loop phosphorylated

(Binding of a cyclin protein and phosphorylation of the T loop activate the Cdk.)

23
Q

What are examples of inactive Cdk?

A
  • T loop in active site
  • Cdk alone
  • Cdk/cyclin bound to p27

(Cdk inhibitors inhibit Cdk.)

24
Q

Cdk inhibitors inhibit the function of cyclin-dependent protein kinases. Different inhibitors display varying mechanisms of Cdk inhibition. Which of the following might a Cdk inhibitor block in order to block Cdk function?
Choose one or more:

  • movement of the T loop into the active site
  • cyclin binding
  • ATP binding
  • substrate binding
A
  • cyclin binding
  • ATP binding
  • substrate binding

(Cdk inhibitors could block cyclin, ATP, or substrate from binding to reduce activity of Cdk.)

25
Q

These two animations illustrate how p53 binds to DNA to regulate transcription, leading to apoptosis of cells and inhibition of cancer cell growth. Several structural regions of p53 contribute to the anti-tumor function. Why is loop 2 important for p53 function?

  • Loop 2 helps position a critical arginine for binding DNA.
  • Loop 2 directly binds to DNA.
  • Loop 2 mediates binding to other transcription factors that help regulate the anti-tumor function of p53.
  • Loop 2 helps coordinate a Ca2+ ion in the Ca2+ finger.
A

Loop 2 helps position a critical arginine for binding DNA.

Loop 2 does not directly bind DNA but instead helps properly position an arginine for DNA binding.

26
Q

The p53 and Tumor Growth animation demonstrates that mice can develop lymphoma in certain tissues lacking p53. Suppose different p53 gene sequences were added back to the lymphoma in mice. For each of the following, predict whether the lymphoma in the mice would grow or shrink over time.

What treatments are associated with tumor growth?

A
  • Add a DNA sequence lacking 90% of the p53 gene
  • Add p53 with Arg248 altered to alanine
  • Add p53 that does not bind Zn2+

(Addition of defective p53 that does not bind Zn2+ or DNA or lacks a major portion of the protein will not cause tumor regression.)

27
Q

The p53 and Tumor Growth animation demonstrates that mice can develop lymphoma in certain tissues lacking p53. Suppose different p53 gene sequences were added back to the lymphoma in mice. For each of the following, predict whether the lymphoma in the mice would grow or shrink over time.

What treatments are associated with tumor regression?

A

-Add a stable p53 that binds better to DNA than wild-type p53

(Only addition of p53 that binds DNA would inhibit tumor growth.)

28
Q

What does the phosphorylation of Cdc25 by M-Cdk do?

  • It activates Cdc25, allowing the cell to exit mitosis.
  • It inactivates Cdc25, which promotes activation of more M-Cdk.
  • It activates Cdc25, which inactivates M-Cdk.
  • It inactivates Cdc25, preventing further activation of M-Cdk.
  • It activates Cdc25, which in turn activates more M-Cdk.
A

It activates Cdc25, which in turn activates more M-Cdk.

(When phosphorylated, Cdc25 becomes activated, which in turn can then remove the inhibitory phosphates from M-Cdk, thereby activating more M-Cdk.)

29
Q

What is true about the phosphorylation of condensins by M-Cdk?

  • It marks them for degradation, allowing chromosomes to decondense.
  • It triggers their assembly onto DNA, compressing chromosomes into a more compact form.
  • It triggers their assembly onto DNA, allowing chromosomes to decondense.
  • It triggers their assembly onto DNA, keeping sister chromatids held together.
  • It marks them for degradation, allowing sister chromatids to separate.
A

It triggers their assembly onto DNA, compressing chromosomes into a more compact form.

(This chromosomal condensation occurs at the start of M phase.)

30
Q

Which of the following statements is false?

  • The pairing of homologous chromosomes during prometaphase is called bi-orientation.
  • Attachment of sister chromatid pairs to opposite poles of the spindle creates tension in the kinetochores, which signals that the sister chromatids are ready to be separated.
  • The cell-cycle control system monitors the tension on the kinetochores to ensure that anaphase does not occur until the sister chromatids are correctly attached to the spindle.
  • Each sister chromatid in a pair must attach to the opposite pole of the spindle for the sister chromatids to be segregated properly.
A

The pairing of homologous chromosomes during prometaphase is called bi-orientation.

(The pairing of homologous chromosomes during prometaphase is not called bi-orientation. Rather, attachment of duplicated chromosomes, or sister chromatids, to microtubules from opposite spindle poles is called bi-orientation.)

31
Q

The anaphase-promoting complex or cyclosome (APC/C) triggers the onset of anaphase by doing which of the following?

  • cleaving spindle microtubules
  • phosphorylating the motor proteins that pull the spindle poles apart
  • triggering the destruction of the cohesins that hold the sister chromatids together
  • triggering the destruction of the condensins that hold the duplicated chromosomes in a condensed state
A

triggering the destruction of the cohesins that hold the sister chromatids together

(The anaphase-promoting complex or cyclosome (APC/C) triggers the onset of anaphase by triggering the destruction of the cohesins that hold the sister chromatids together. This release allows the chromatids to be pulled toward the opposite poles of the dividing cell.)

32
Q

How many kinetochores are present in a human cell during mitosis?

  • 2
  • 23
  • 46
  • thousands
  • 92
A

92

(During mitosis, 92 kinetochores are present in a human cell. Human cells have 46 total chromosomes, each of which has two kinetochores after duplication.)

33
Q

The goal of gene-therapy techniques is to provide cells with functional copies of mutated genes. One technique involves introducing functional genes on an “artificial chromosome.” Somatic cells in which the artificial chromosome has been inserted have 47 chromosomes instead of the normal 46 (i.e., for human cells). To be effective, the artificial chromosome must be passed to daughter cells during mitosis, which requires that the artificial chromosome contain sequences on which kinetochores can assemble. With this in mind, what should designers of artificial chromosomes include to ensure proper kinetochore assembly on the artificial chromosome?

  • centromere
  • origin of replication
  • condensin
  • centrosome
A

Centromere

(The centromere is the chromosomal region upon which kinetochores assemble. Microtubules responsible for separating duplicated chromosomes attach to kinetochores.)

34
Q

Kinesin-5 is a motor protein that binds to overlapping interpolar microtubules near the midzone of the mitotic spindle. Each of these kinesin proteins has two motor domains that walk toward the plus ends of the microtubules to which the kinesin is bound. When is this kinesin active and how does it affect the spindle?

  • During anaphase B, kinesin-5 slides the microtubules past one another toward the spindle poles, pulling the poles together and shortening the spindle.
  • During anaphase B, kinesin-5 slides the microtubules past one another toward the spindle poles, pushing the poles apart and lengthening the spindle.
  • During anaphase A, kinesin-5 slides the microtubules past one another toward the spindle poles, pushing the poles apart and lengthening the spindle.
  • During anaphase A, kinesin-5 slides the microtubules past one another toward the spindle poles, pulling the poles together and shortening the spindle.
  • During anaphase B, kinesin-5 slides the microtubules over one another toward the spindle equator, pulling the poles together and shortening the spindle.
A

During anaphase B, kinesin-5 slides the microtubules past one another toward the spindle poles, pushing the poles apart and lengthening the spindle.

(During anaphase B, kinesin-5 slides the microtubules past one another toward the spindle poles, pushing the poles apart and lengthening the spindle. The free, plus ends of interpolar microtubules lie near the spindle midzone. Because kinesin-5 moves toward the plus ends of microtubules, it will slide the interpolar microtubules past one another toward the spindle poles. This sliding will push the poles apart, lengthening the spindle.)

35
Q

It is often useful for scientists to study a population of cells that are all at the same stage of the cell cycle. For example, the discovery of cyclins and Cdks was enabled by studying frog eggs that divided synchronously after fertilization; extracts from the embryos were thus representative of the cell-cycle stage at which the extract was made. Researchers have devised means to synchronize asynchronous populations of cultured cells. For example, serum starvation deprives cells of mitogens and blocks cells in the G0/G1 phase of the cell cycle. Another method involves gently shaking culture flasks and harvesting the cells that release from the substratum. In what stage of the cell cycle are these cells most likely to be?

  • G2 phase
  • M phase
  • G1 phase
  • S phase
A

M phase

(As cells enter M phase, they become rounded and decrease adherence to other cells and the substratum. Shaking of the culture flask, a technique known as mitotic shake-off, releases these loosely attached M-phase cells into the culture media. For information on mitotic shake-off and other techniques for obtaining synchronized cells, see the article “Methods for synchronizing cells at specific stages of the cell cycle”)

36
Q

One approach to killing cancer cells is to induce apoptosis. Which of the following are reasonable approaches that researchers can take to induce apoptosis in cancer cells?
Choose one or more:

  • inhibiting the Bcl2 protein
  • inhibiting the G1-cyclin-dependent kinase protein
  • inhibiting the p53 protein
  • activating the Bax protein
A
  • inhibiting the Bcl2 protein
  • activating the Bax protein

(Caspase activation is regulated by the Bcl2 family of proteins. Some proteins in this family, such as Bax, stimulate apoptosis, while others, such as Bcl2, inhibit apoptosis. Researchers have tried inducing apoptosis by both activating Bax proteins and inhibiting Bcl2 proteins.)

37
Q

Mutations that prevent Bcl2 family proteins Bax and Bak from interacting with the outer mitochondrial membrane would have which effect?

  • preventing the release of cytochrome c and triggering the activation of procaspase-9
  • preventing the release of cytochrome c and promoting the assembly of the apoptosome
  • triggering the release of cytochrome c and promoting the assembly of the apoptosome
  • preventing the release of cytochrome c and inhibiting apoptosis
  • triggering the release of cytochrome c and promoting apoptosis
A

preventing the release of cytochrome c and inhibiting apoptosis

(Bax and Bak trigger the release of cytochrome c and promote apoptosis; mutations that impair their ability to interact with the outer mitochondrial membrane would inhibit these actions.)

38
Q

Soon after nerve growth factor (NGF) was discovered, investigators injected newborn mice with antibodies that inactivated it. Compared to control mice, those that received the antibody showed massive amounts of nerve cell death. After a week of daily antibody injections, up to 99% of the neurons in certain parts of the nervous system of these mice were gone. What do these results suggest?

  • NGF is a survival factor for developing neurons.
  • NGF triggers apoptosis in developing neurons.
  • NGF cannot protect developing neurons from death by apoptosis.
  • NGF is a mitogen that promotes the proliferation of developing neurons.
  • NGF signaling is sufficient for survival of developing neurons.
A

NGF is a survival factor for developing neurons.

(Based on these observations, NGF is most likely a survival factor for developing neurons. Treating mice with NGF antibodies inactivates NGF. The massive increase in cell death after this treatment suggests that NGF is important for nerve cell survival, as cells undergo apoptosis when deprived of NGF.)

39
Q

Investigators interested in studying the activation of apoptosis inject cytochrome c into the cytosol of two types of mammalian cells: cells that are normal and cells in which Bak and Bax have been inactivated by mutation.
How would these cells be predicted to respond?

  • The normal cells will undergo apoptosis and the mutant cells will continue to grow.
  • The mutant cells will undergo apoptosis and the normal cells will continue to grow.
  • Neither cell type will undergo apoptosis, so both will continue to grow.
  • The normal cells will undergo apoptosis and the mutant cells will die by necrosis.
  • Both cell types will undergo apoptosis.
A

Both cell types will undergo apoptosis.

(Bak and Bax promote cell death by triggering the release of cytochrome c into the cytosol. Injecting cytochrome c into the cytosol thus bypasses the action of Bak and Bax, triggering the assembly of the apoptosome and initiating apoptosis in both mutant and normal cells.)

40
Q

Which of the following structural changes is not typically seen in a cell that is undergoing apoptosis?

  • The cell swells.
  • The nuclear envelope disassembles.
  • The cell develops irregular bulges.
  • The cytoskeleton collapses.
A

The cell swells.

(Apoptotic cells actually shrink and condense. Cells that die by necrosis typically swell and burst, spilling their contents over their neighbors. Apoptotic cells die neatly, without damaging their neighbors.)