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BM 210: Introduction to Biochemistry > Block E Part 1: Cell Division, Cell Growth and Control Mechanisms > Flashcards

Block E Part 1: Cell Division, Cell Growth and Control Mechanisms Flashcards

1
Q

What is the basic function of the cell cycle?

A

To duplicate DNA in the chromosomes and then segregate the copies into 2 identical daughter cells
(Lecture 1, Slide 5)

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2
Q

What phase of the cell cycle does chromosome duplication occur in?

A

S phase - S for DNA synthesis
(Lecture 1, Slide 5)

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3
Q

How long does the S phase of the cell cycle last and how long is this compared to the full cycle?

A

~ 10-12 hours and is roughly half the time of the full cycle
(Lecture 1, Slide 5)

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4
Q

What phase of the cell cycle does chromosome segregation and cell division occur in?

A

M - M for mitosis
(Lecture 1, Slide 5)

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5
Q

How long does the M phase of the cell cycle last?

A

~ 1 hour
(Lecture 1, Slide 5)

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6
Q

What are the 2 major events that make up the M phase of the cell cycle?

A

Mitosis (aka nuclear division) and cytokinesis (aka cytoplasmic division)
(Lecture 1, Slide 6)

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7
Q

What helped us understand how the cell cycle worked?

A

Model organisms
(Lecture 1, Slide 7)

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8
Q

What is the order of the 4 phases of the cell cycle?

A

G1->S->G2->M
(Lecture 1, Slide 8)

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9
Q

Why does the cell cycle have controls?

A

To ensure that progression in the cell cycle only occurs in the right situations
(Lecture 1, Slide 8)

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10
Q

What are the 3 main control points of the cell cycle?

A

Start transition
G2/M transition
Anaphase onset/cytokinesis
(Lecture 1, Slide 8)

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11
Q

What power do the controls points in the cell cycle have?

A

The power to stop cell division until any problem in the cell cycle is resolved
(Lecture 1, Slide 8)

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12
Q

What is Schizosaccharomyces pombe?

A

Fission yeast
(Lecture 1, Slide 9)

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13
Q

What was used to isolate mutants blocked at various stages of the cell cycle in Schizosaccharomyces pombe?

A

Yeast genetics
(Lecture 1, Slide 9)

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14
Q

What type of mutants did Nurse and Hartwell use in Schizosaccharomyces pombe?

A

Mutants that were temperature sensitive
(Lecture 1, Slide 9)

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15
Q

What are temperature sensitive mutants?

A

Mutations that produce a protein that functions at one temperature, but not another
(Lecture 1, Slide 9)

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16
Q

What type of mutant is a temperature sensitive mutant?

A

A conditional mutant
(Lecture 1, Slide 9)

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17
Q

What is Xenopus laevis?

A

African clawed frog
(Lecture 1, Slide 11)

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18
Q

What is a useful model system to study the cell cycle?

A

Egg development in the Xenopus laevis frog
(Lecture 1, Slide 11)

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19
Q

Why do Xenopus oocytes (eggs from the African clawed frog) become arrested in the G2 phase of the cell cycle for 8 months?

A

So they can grow in size to a diameter of 1 mm, stockpiling molecules required post-fertilisation to generate a swimming, feeding tadpole
(Lecture 1, Slide 11)

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20
Q

How do the Xenopus oocytes cells of African clawed frogs arrested in the G2 phase of the cell cycle begin meiosis?

A

When stimulated by a male, the female ovarian cells secret progesterone, which induces the arrested cells to enter meiosis
(Lecture 1, Slide 11)

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21
Q

What occurs during meiosis of xenopus laevis (African clawed frogs)?

A

The diploid oocyte (egg) produces mature eggs which are ready to be fertilised by sperm
(Lecture 1, Slide 11)

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22
Q

What does fusion of the sperm and egg generate in Xenopus oocytes and what does it start?

A

A diploid nucleus, and embryogenesis proceeds with multiple rounds of the cell cycle
(Lecture 1, Slide 11)

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23
Q

Why is it possible to remove the cytoplasm from one cell of xenopus oocytes and mature eggs and introduce it into another?

A

Due to their large size
(Lecture 1, Slide 11)

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24
Q

How can populations of cells be studied?

A

By measuring the DNA content of the individual cells in a flow cytometer
(Lecture 1, Slide 15)

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25
Q

How can you tell how much DNA is in a cell and how many cells are present?

A

Cells are incubated with Hoechst-33342, a membrane-permeant dye that fluoresces when it binds to DNA; the amount of fluorescence is directly proportional to the amount of DNA in each cell
(Lecture 1, Slide 15)

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26
Q

What are the 3 peaks identified in cell population when DNA content is analysed with a flow cylinder?

A

Those that have an un-replicated complement of DNA and are therefore in G1
Those that have a fully replicated complement of DNA (twice the G1 DNA content) and are in G2 or M phase
Those that have an intermediate amount of DNA and are in S phase
(Lecture 1, Slide 16)

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27
Q

How can we study cell cycle regulation?

A

Study the localisation of protein (or mutants) in cells in culture using indirect immunofluorescence microscopy
(Lecture 1, Slide 17)

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28
Q

What does the cell-cycle control system depend on?

A

Cyclically activated Cyclin-dependent protein kinases (Cdks)
(Lecture 1, Slide 19)

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29
Q

What does each Cdk-cyclin complex do?

A

Phosphorylates a different set of proteins
(Lecture 1, Slide 21)

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30
Q

How can the same cyclin-Cdk complex can induce different effects at different times of the cell cycle?

A

As accessibility to targets may change in a cell cycle-dependent manner
(Lecture 1, Slide 21)

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31
Q

What can cyclins direct to specific substrates?

A

The kinase
(Lecture 1, Slide 21)

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32
Q

How is the next phase of the cell cycle started and stopped if needed?

A

The Cdk without cyclin is inactive - cell cycle is stopped. The cyclin activates the Cdk which phosphorylates its targets, beginning the next phase
(Lecture 1, Slide 22)

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33
Q

How do cdks become partially active?

A

In the absence of the cell cycle cdks show a loop (T-loop) which blocks access of substrates to the kinase active site , cyclin binding causes this loop to move aside which partially activates the kinase
(Lecture 1, Slide 23)

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34
Q

How do Cdks become fully active?

A

Full activation requires a Cdk-activating kinase to phosphorylate the T-loop driving a further change in conformation, making the Cdk now fully active
(Lecture 1, Slide 23)

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35
Q

What triggers the metaphase to anaphase transition?

A

Regulated proteolysis
(Lecture 1, Slide 28)

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36
Q

What drives progression through the start and G2/M transitions?

A

Specific cyclin-Cdk complexes
(Lecture 1, Slide 28)

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37
Q

What triggers progression through the metaphase-to-anaphase transition?

A

Protein destruction
(Lecture 1, Slide 28)

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38
Q

What is the key regulator in the metaphase to anaphase transition?

A

Anaphase promoting complex (sometimes called cyclosome; APC/C)
(Lecture 1, Slide 28)

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39
Q

What is anaphase promoting complex?

A

A member of the ubiquitin ligase family of enzymes
(Lecture 1, Slide 28)

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40
Q

What is ubiquitin?

A

A small protein added to proteins by the concerted action of three enzymes; E1, E2 and E3 - this is called uniquitylation
(Lecture 1, Slide 29)

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41
Q

What is polyubiquitylation a trigger for?

A

Proteins to be degraded in cells
(Lecture 1, Slide 29)

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42
Q

What does polyubiquitin target proteins to?

A

The proteasome
(Lecture 1, Slide 29)

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43
Q

What does the proteasome do to proteins?

A

It chews them up and allows the amino acids to be re-used
(Lecture 1, Slide 29)

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44
Q

What happen to proteins in the proteasome after they are chewed up?

A

Ubiquitin is cleaved off and is recycled by the cell
(Lecture 1, Slide 29)

45
Q

What are 2 examples of enzymes that can function as the E3 enzyme to help make ubiquitin?

A

Anaphase promoting complex (APC/C)
SCF
(Lecture 1, Slide 29)

46
Q

What does anaphase promoting complex (APC/C) catalyse?

A

The ubiquitylation and destruction of two major types of proteins; Securin and S- and M-cyclins
(Lecture 1, Slide 31)

47
Q

Why does APC/C catalyse the ubiquitylation and destruction of securin?

A

Securin holds the sister chromatids together, separating the sister chromatids starts anaphase, which is accomplished by destroying securin
(Lecture 1, Slide 31)

48
Q

Why does APC/C catalyse the ubiquitylation and destruction of S- and M-cyclins?

A

To stop the cell cycle progressing
(Lecture 1, Slide 31)

49
Q

When does APC/C activity significantly increase?

A

When it associates with an activating subunit such as Cdc20
(Lecture 1, Slide 33)

50
Q

When is Cdc20 concentration elevated and by what control?

A

By the action of Cdk-M through feedback control
(Lecture 1, Slide 33)

51
Q

What does the APC/C-Cdc20 complex (acting as an “E3” recruit and why?

A

Ubiquitylation enzymes E1 and E2 to target a specific protein
(Lecture 1, Slide 33)

52
Q

What does a protein being ubiquitylated signal?

A

The cell to destroy that protein
(Lecture 1, Slide 33)

53
Q

When in the cell cycle is SCF active?

A

Constantly
(Lecture 1, Slide 35)

54
Q

What does SCF do to CKI proteins late in G1 phase?

A

It poly-ubiquitylates them
(Lecture 1, Slide 35)

55
Q

What does SCF poly-ubiquitylating CKI proteins in G1 control?

A

Activation of S-Cdks and DNA replication
(Lecture 1, Slide 35)

56
Q

What is ubiquitylation by SCF controlled by?

A

Changes in phosphorylation of its targets, recognised by associated F-box proteins which can only bind phospho-targets
(Lecture 1, Slide 35)

57
Q

What stimulates the activation of G1-Cdk?

A

Various external and internal signals
(Lecture 1, Slide 36)

58
Q

What does the activation of G1-Cdk in turn stimulate?

A

The expression of genes encoding G1/S and S-cyclins
(Lecture 1, Slide 36)

59
Q

What does the activation of G1/S-Cdk drive?

A

Progression through the start transition
(Lecture 1, Slide 36)

60
Q

How does G1/S-Cdk’s initiate S phase?

A

They unleash a wave of S-Cdk activity, which initiates chromosome duplication in S phase
(Lecture 1, Slide 36)

61
Q

What does M-Cdk activation trigger?

A

Progression through the G2/M transition and the events of early mitosis leading to the alignment of sister chromatid pairs at the equator of the mitotic spindle
(Lecture 1, Slide 36)

62
Q

What 2 things make up the total cell mass?

A

Total number of cells and their size
(Lecture 1, Slide 37)

63
Q

What does cell number depend on?

A

The amount of cell divisions and death
(Lecture 1, Slide 37)

64
Q

What do mitogens stimulate?

A

Cell division
(Lecture 1, Slide 38)

65
Q

What do growth factors stimulate?

A

Cell growth
(Lecture 1, Slide 38)

66
Q

What is cell growth?

A

An increase in cell mass
(Lecture 1, Slide 38)

67
Q

What do survival factors do?

A

Support cell survival by suppressing programmed cell death (apoptosis)
(Lecture 1, Slide 38)

68
Q

What do some human cells that do not divide do instead?

A

Terminally differentiate
(Lecture 1, Slide 38)

69
Q

What limitation do many human cells have built into them?

A

How many times they can divide
(Lecture 1, Slide 38)

70
Q

How did the path of isolation of platelet-derived growth factor start?

A

With the observation that fibroblasts in a culture dish proliferate when provided with serum but not when provided with plasma
(Lecture 1, Slide 39)

71
Q

How is plasma prepared?

A

Plasma is prepared by removing the cells from blood without allowing clotting to occur
(Lecture 1, Slide 39)

72
Q

How is serum prepared?

A

By allowing blood to clot and taking the cell-free liquid that remains
(Lecture 1, Slide 39)

73
Q

What happens when blood clots?

A

Platelets incorporated in the clot are stimulated to release the contents of their secretory vesicles
(Lecture 1, Slide 39)

74
Q

What suggested that platelets contain one or more mitogens?

A

The superior ability of serum to support cell proliferation
(Lecture 1, Slide 39)

75
Q

How was the hypothesis that platelets contain one or more mitogens confirmed and what was the crucial factor?

A

By showing that extracts of platelets could server instead of serum to stimulate fibroblast proliferation, and crucial factor in the extracts was shown to be a protein, which was purified and named platelet-derived growth factor (PDGF)
(Lecture 1, Slide 39)

76
Q

What does PDGF liberated from blood clots help stimulate?

A

Cell division during wound healing
(Lecture 1, Slide 39)

77
Q

How many mitogens does our body have and why?

A

Around 50, to stimulate a broad range of cells types
(Lecture 1, Slide 39)

78
Q

How do mitogens control the rate of cell division?

A

By acting in the G1 phase of the cell cycle
(Lecture 1, Slide 40)

79
Q

What do mitogens interact with?

A

Cells surface receptors
(Lecture 1, Slide 40)

80
Q

What do mitogens interacting with cell-surface receptors trigger?

A

Multiple intracellular signalling pathways
(Lecture 1, Slide 40)

81
Q

What does the activation of the small GTPase Ras lead to?

A

Activation of MAP kinase cascade
(Lecture 1, Slide 40)

82
Q

What does activation of a MAP kinase cascade lead to?

A

Increase expression of numerous immediate early genes, including the gene encoding the transcription of the regulatory protein Myc
(Lecture 1, Slide 40)

83
Q

What is Myc thought to promote and what does it stimulate?

A

It promotes cell-cycle entry and plays a major role in stimulating the transcription of genes that increase cell growths
(Lecture 1, Slide 41)

84
Q

What is one of the mechanisms that Myc uses to promote cell entry?

A

It increases the expression of genes encoding G1 cyclins (D cyclins) thereby increasing G1-Cdk activity
(Lecture 1, Slide 41)

85
Q

What is the key function of G1-cdk complexes in animal cells?

A

To activate a group of gene regulatory factors called the E2F proteins
(Lecture 1, Slide 41)

86
Q

What to E2F proteins do?

A

They bind to specific DNA sequences in the promoters of a wide variety of genes that encode proteins required for S-phase entry, such as G1/S-cyclins and proteins involved in DNA synthesis and chromosome duplication
(Lecture 1, Slide 41)

87
Q

What happens to E2F-dependent gene expression in the absence of mitogen stimulation?

A

It is inhibited by an interaction between E2F and members of the retinoblastoma protein (Rb) family.
(Lecture 1, Slide 41)

88
Q

When cells are stimulated to divide by mitogens, what does active G1-Cdk do to retinoblastoma (Rb) family members and what does this result in?

A

G1-Cdk accumulates, and phosphorylates Rb family members which reduces their binding to E2F, which then leads them to activate expression of their target genes
(Lecture 1, Slide 41)

89
Q

What does abnormally proliferation signals cause and what is the exception?

A

Cell-cycle arrest or apoptosis, except in cancer cells
(Lecture 1, Slide 42)

90
Q

Why were many genes that code for components of the mitogenic signalling pathways originally identified as cancer-promoting genes?

A

As mutations in them contribute to the development of cancer
(Lecture 1, Slide 42)

91
Q

What does a single amino acid mutation in the GTPase Ras cause?

A

The protein to become permanently overactive
(Lecture 1, Slide 42)

92
Q

What does the GTPase Ras becoming permanently overactive lead to?

A

Constant stimulation of Ras-depending signalling pathways, even in the absence of mitogenic stimulation
(Lecture 1, Slide 42)

93
Q

What do mutations that cause an overexpression of Myc stimulate and therefore promote?

A

Excessive cell growth and proliferation, promoting the development of cancer
(Lecture 1, Slide 43)

94
Q

What are 2 possible results of experimentally overproducing a hyperactive form of Ras or Myc in most normal cells?

A

Instead of excessive proliferation, cells undergo either permanent cell-cycle arrest or apoptosis
(Lecture 1, Slide 42)

95
Q

What does most normal cells going into permanent cell-cycle arrest or apoptosis in response to an experimental overproduction of a hyperactive form of Ras or Myc prove?

A

That the normal cell seems to be able to detect abnormal mitogenic stimulation, and it can respond by preventing further division
(Lecture 1, Slide 42)

96
Q

What is Mdm2?

A

It is a E3 ubiquitin ligase
(Lecture 1, Slide 43)

97
Q

What is the main function of Mdm2?

A

To ubiquitinate P53, signalling it for destruction by the proteosome
(Lecture 1, Slide 43)

98
Q

What does abnormally high levels of Myc activate?

A

Arf
(Lecture 1, Slide 43)

99
Q

What do Arf do once activated by Myc?

A

It binds and inhibits Mdm2, increasing p53 levels
(Lecture 1, Slide 43)

100
Q

What 2 scenarios can P53 cause once activated and what 2 things decide which one it picks?

A

It can either cause cell-cycle arrest or apoptosis depending on the cell type and extracellular conditions
(Lecture 1, Slide 43)

101
Q

What is cell proliferation accompanied by?

A

Cell growth - there is little point in telling a cell to divide if it is not triggered to grow
(Lecture 1, Slide 44)

102
Q

What does a growth factor binding to a cell surface receptor activate?

A

PI 3-kinase
(Lecture 1, Slide 44)

103
Q

What does PI 3-kinase promote?

A

Protein synthesis
(Lecture 1, Slide 44)

104
Q

How does Pi 3-kinase promote protein synthesis?

A

Through a complex signalling pathway that leads to the activation of the protein kinase TOR
(Lecture 1, Slide 44)

105
Q

On top of the signalling pathway PI 3-kinase uses to activate TOR, what else can help activate it?

A

Extracellular nutrients such as amino acids
(Lecture 1, Slide 44)

106
Q

How does TOR stimulate protein synthesis?

A

By phosphorylating a range of transcription regulatory proteins leading which contribute to an increased production of ribosomes
(Lecture 1, Slide 45)

107
Q

In addition to binding to cell surface receptors to activate PI 3-kinase what do growth factors stimulate increase production of?

A

Myc
(Lecture 1, Slide 45)

108
Q

How does Myc help promote cell metabolism and growth after it’s production is increased by growth factor stimulation?

A

By activating the transcription of various genes that promote cell metabolism and growth
(Lecture 1, Slide 45)

109
Q
A

BM 210: Introduction to Biochemistry (12 decks)

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