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Cell Bio > L16. Cell Cycle I and II and cancer > Flashcards

L16. Cell Cycle I and II and cancer Flashcards

1
Q

explain the four phases of the eukaryotic cell cycle

A
  1. M phase (mitosis and cytokinesis)
  2. interphase (G1 phase, S phase, and G2 phase)
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2
Q

eukaryotic cell cycle - M phase

A
  • mitosis: nuclear division
  • cytokinesis: cytoplasmic division
  • lasts about an hour (small fraction of total cell cycle)
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3
Q

eukaryotic cell cycle - interphase

A
  • period between 1 m phase and the next
  • cell growth
  • DNA is replicated
  • centrosome is duplicated
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4
Q

eukaryotic cell cycle: interphase - G1 and G2 phase

A
  • gap phases that flank s phase
  • monitors cell’s environment
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5
Q

eukaryotic cell cycle: interphase - S phase

A

synthesis and replication of DNA

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6
Q

explain the cell cycle control system

A
  • it ensures that key processes occur sequentially
  • does this via checkpoints
  • cycle may arrest or move to G0 (specialized resting state) if conditions are not met
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7
Q

cell cycle control system - what is the system dependent on

A
  • cyclically activating and inactivating proteins
  • called cyclin-dependent kinase (Cdk) and cyclin
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8
Q

cell cycle control system - explain Cdks

A
  • it is regulated by phosphorylation and dephosphorylation
  • Cdk is switched on by cyclins
  • once activated, Cdks trigger entry into S or M phase
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9
Q

cell cycle control system - explain cyclin

A
  • they are regulated by transcription and proteolysis (breakdown of protein)
  • they do not have enzymatic activity but are required for activation of kinase
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10
Q

Cdk and cyclins - explain the relationship between Cdk activity and cyclin concentration

A
  • accumulation of cyclins during mitosis, helps regulate Cdk activity
  • increase in cyclins = increased activity in Cdks
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11
Q

Cdks and cyclins - how are different cell cycle events triggered

A
  • different Cdks associate with different cyclins
  • M-cyclins associate with M-Cdks to activate M phase
  • S cyclins and G1/S cyclins associate with S-Cdks and G1/S-Cdks to activate S phase
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12
Q

how are Cdks activated

A
  1. dephosphorylation
  2. positive feedback
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13
Q

Cdk activation - dephosphorylation

A
  • Cdks have inhibitory phosphates
  • to become active, they must be dephosphorylated
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14
Q

Cdk activation - positive feedback

A
  • once the M-Cdk is active, it propagates the activation of more M-Cdk by activating the activating phosphatase (Cdc25)
  • M-Cdk will accumulate through the G2 phase and will quickly move the cell from G2 to M phase
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15
Q

how is Cdk inactivated

A
  1. cyclin degradation via ubiquitin-tagged degradation
  2. use of transcriptional regulator p53
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16
Q

Cdk inactivation - explain ubiquitin-tagged degradation of cyclin

A
  • degradation of M cyclins are mediated by anaphase promoting complex (APC)
  • this complex will tag cyclins with ubiquitin and the cyclin will be feed into a proteasome chamber for degradation
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17
Q

Cdk inactivation - use of transcriptional regulator p53

A
  • used in G1 checkpoint in response to DNA damage
  • damage results in increased levels and function of p53
  • p53 activates the gene expression of the Cdk inhibitor p21
  • p21 will then bind to G1/S- and S-Cdks to cause the cycle to be arrested in G1 to repair DNA
  • if the damage is too severe, p53 can induce apoptosis
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18
Q

where are the checkpoints in the cell cycle located

A
  • checkpoint in mitosis
  • G1 checkpoint
  • G2 checkpoint
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19
Q

cell cycle checkpoints - checkpoint in mitosis

A
  • are all chromosomes properly attached to the mitotic spindle?
  • if yes, then the duplicated chromosomes are pulled apart
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20
Q

cell cycle checkpoint - G1 checkpoint

A
  • is the environment favorable
  • if yes, the cell will enter S phase
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21
Q

cell cycle checkpoint - G2 checkpoint

A
  • is all DNA replicated?
  • is all DNA damage repaired?
  • if yes to both, the cell enters mitosis
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22
Q

cell cycle checkpoint: if conditions are not met - checkpoint in mitosis

A

inhibition of anaphase promoting complex activation delays exit from mitosis

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23
Q

cell cycle checkpoint: if conditions are not met - G1 checkpoint

A
  • Cdks inhibitors block entry to s phase
  • DNA damage causes increased levels and function of p53
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24
Q

cell cycle checkpoint: if conditions are not met - G2 checkpoint

A

inhibition of activating phosphatase (Cdc25) blocks entry to mitosis

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25
Q

explain how mitogens promote cyclin production

A
  • they elicit cell signaling and the cycling will activate G1 cyclins, G1/S cyclins, and DNA synthesis proteins
  • it has a negative control retinoblastoma (Rb) that keeps transcriptional factors inactive
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26
Q

mitogens and cyclin production - what happens to Rb after Cdks are activated

A
  • the Cdks will phosphorylate Rb and Rb will release the transcription regulators
  • the regulators then activate genes required for cell proliferation
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27
Q

what are the two steps of initiating DNA replication

A
  1. origin loaded
  2. origin fired
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28
Q

initiating DNA replication - origin loaded

A
  • happens in G1 phase
  • the origin of replication serves as landing pads for proteins
  • the origin recognition complex (ORC) is perched on top of the replication origin and recruits Cdc6
  • DNA helicase is loaded to open up the double helix
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29
Q

initiating DNA replication - origin fired

A
  • happens in S phase
  • helicase and the ORC = replication complex
  • S-Cdk activates DNA helicase and promotes replication fork formation
  • and then DNA replication begins
  • S-Cdk also helps prevent re-replication by phosphorylating Cdc6
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30
Q

what are cohesins

A
  • immediately after s phase DNA replication, sister chromatids are remained tightly bound by cohesins
  • defective cohesins lead to chromosomal segregation problems
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31
Q

explain the stages of mitosis

A
  1. prophase
  2. prometaphase
  3. metaphase
  4. anaphase
  5. telophase
32
Q

mitosis- prophase

A
  • duplicated chromosomes condense due to condensins
  • mitotic spindle assembles between two centrosomes
33
Q

mitosis: prophase - condensins

A
  • condensin complex formation is triggered by M-Cdk phosphorylation
  • the protein complexes facilitates chromosome condensation
  • this makes it easier for them to be segregated during mitosis
34
Q

mitosis: prophase - how are mitotic spindles formed

A
  • at the start of mitosis, stability of microtubules decrease and causes dynamic instability
  • motor proteins and associated proteins cross-link the overlapping microtubules
  • this interaction stabilizes the (+) ends
  • M-Cdks phosphorylate microtubule proteins
  • and the centrosomes act as the spindle poles
35
Q

mitosis - prometaphase

A
  • starts with the breakdown of the nuclear envelope via phosphorylation of nuclear pore proteins and lamins
  • chromosomes attach to spindle microtubules
36
Q

mitosis: prometaphase - how are the chromosomes attached to the mitotic spindle

A
  • spindle microtubules attach at kinetochores
  • this attachment generates tension on the kinetochores
  • the tension signals to the kinetochores that they are attached correctly
  • the cell cycle control system monitors this tension
37
Q

mitosis: prometaphase - define kinetochores

A

protein complexes that assemble on the centromere of each condensed chromosome

38
Q

mitosis: prometaphase - what are the three classes of microtubules that make up the mitotic spindle

A
  1. aster microtubules
  2. kinetochore microtubules
  3. interpolar microtubules
39
Q

mitosis: three classes of microtubules that make up the mitotic spindle - aster microtubules

A

any microtubule originating from the centrosome which does not connect to a kinetochore.

40
Q

mitosis: three classes of microtubules that make up the mitotic spindle - kinetochore microtubules

A

capture each pair of sister chromatids at their kinetochores

41
Q

mitosis: three classes of microtubules that make up the mitotic spindle - interpolar microtubules

A

cross-linked at overlaps throughout the spindle

42
Q

mitosis - metaphase

A
  • chromosomes are aligned at the metaphase plate
  • kinetochore microtubules attach to opposite poles of the spindles
43
Q

mitosis - anaphase

A
  • begins by cohesin breakage
  • sister chromatids separate
  • kinetochore microtubules shorten and spindle poles move apart
44
Q

mitosis: anaphase - what is the anaphase promoting complex (APC)

A
  • it triggers the separation of sister chromatids by promoting cohesin destruction
  • cohesin linkage is destroyed via separase
  • separase is held inactive by securin
  • securin is destroyed by APC via ubiquitin targeting and allows seperase to cleave cohesin
45
Q

mitosis: anaphase - how are sister chromatids seperated

A
  1. anaphase A
  2. anaphase B
46
Q

mitosis: anaphase - explain anaphase A

A

kinetochore microtubules shorten and the attached chromosomes move poleward

47
Q

mitosis: anaphase - explain anaphase B

A

the spindle poles move themselves apart

48
Q

mitosis - telophase

A
  • chromosomes arrive at opposite poles
  • nuclear envelope reassembles
  • division of cytoplasm begins with assembly of contractile ring
49
Q

mitosis: telophase - explain the reassembly of the nuclear envelope

A
  • nuclear pore proteins and lamins are now dephosphorylated
  • allows them to be reassembled
  • pores pump in nuclear proteins and the nucleus expands
50
Q

explain cytokinesis

A

cytoplasm is divided in two by contractile ring of actin and myosin filaments

51
Q

cytokinesis - explain the cleavage furrow

A
  • the first visible sign of cytokinesis
  • occurs in a plane that runs perpendicular to the mitotic spindle
  • this positioning ensures that the furrow cuts between the two groups of segregated chromosomes
52
Q

cytokinesis - how does the contractile ring divide the cell

A
  • the ring is composed of overlapping actin and myosin filaments
  • it is attached to membrane-associated proteins on the cytoplasmic face of the PM
  • the force of the ring is generated by the sliding of actin filaments against myosin filaments
53
Q

what is apoptosis

A
  • programmed cell death
  • it is used for: development, organ reorganization, metamorphosis, and immunity
54
Q

apoptosis - how is it quick and clean

A
  • a cell that dies may swell and burst and can trigger a potentially damaging response
  • to combat this, phagocytic cells (macrophages) will engulf the cell before it spills its contents
  • and it allows the organic components to be recycleda
55
Q

apoptosis - explain caspase cascades

A
  • pro-caspases are activated in response to apoptosis signals and they are activated through cleavage and assembly
  • initiator caspases cleave and activate downstream executioner caspases which may activate more executioner caspases
56
Q

apoptosis: caspase cascades - explain the proteolytic cascade

A
  • they cause the breakdown of key cellular proteins
  • which then causes the irreversible breakdown of the nuclear lamina
  • nucleases will come and break DNA
  • finally, the apoptotic cell is cleaned up
57
Q

explain intrinsic apoptosis

A
  • mediated by the Bcl2 family which regulates caspase activation
  • death promoting proteins are Bax and Bak
  • the proteins are activated in response to DNA damage and they facilitate cytochrome c release from the mitochondria
58
Q

intrinsic apoptosis - how will apoptosis be prevented or activated

A
  • prevented: Bcl2 protein inhibits apoptosis by preventing Bax/Bak mediated cytochrome c release
  • activated: cytochrome c molecules activate initiator procaspases by promoting the assembly of an apoptosome
  • apoptosome then recruits a initiator procaspase that triggers apoptosis
59
Q

explain extrinsic apoptosis

A
  • death receptor Fas is activated by a membrane bound protein called Fas ligand
  • this ligand is present on the surface of specialized immune cells called killer lymphocytes
  • binding of Fas ligand to its receptor triggers assembly of a death-inducing signaling complex
  • this complex then induces initiator procaspases
60
Q

what are the three major categories of positively acting signal proteins

A
  1. survival factors
  2. mitogens
  3. growth factors
61
Q

positively acting signal proteins - survival factors

A
  • promote cell survival by suppressing apoptosis
  • limited survival factor release dictates signaling/target cell ratios
  • they upregulate the expression of anti-apoptotic proteins
  • Bcl2 regulation
62
Q

positively acting signal proteins - mitogens

A
  • stimulates cell division by overcoming cell cycle blocks
  • it inhibits Rb so cell proliferation genes can be expressed
63
Q

positively acting signal proteins - growth factors

A
  • stimulate cell growth by promoting synthesis and inhibiting degradation of macromolecules
  • not dependent on cell cycle control
  • terminally differentiated cells (nerve, muscle, immune) do most of their growing after they have been differentiated and have stopped dividing
  • most extracellular growth factors bind to cell surface receptors to induce events
64
Q

explain the properties of a cancer cell

A
  1. proliferation
  2. invasion
  3. metastasis
65
Q

properties of a cancer cell - proliferation

A
  • the cell itself and its progeny proliferate in defiance of the normal cell constraints
  • can form a tumor (clustered cancer cells that form a single mass)
66
Q

properties of a cancer cell - invasion

A

the cell invades and colonizes territories normally reserved for other cells

67
Q

properties of a cancer cell - metastasis

A

tumor cells with invasive properties can break loose from the primary tumor and form secondary tumors (metastases)

68
Q

what may cause genetic instability

A
  • defects in DNA replication
  • defects in DNA repair
  • defects in cell-cycle checkpoint mechanisms
  • mistakes in mitosis
  • abnormal chromosome numbers
69
Q

explain the process of tumorigenesis

A
  • a single cell undergoes a mutation that enhances its ability to proliferate, survive, or both
  • this cell becomes the dominant clone in the tumor
  • the cell then evolves by repeated rounds of mutation, proliferation, and natural selection
70
Q

tumorigenesis - dominant mutation

A
  • oncogenes (Ras)
  • gain of function mutation in a single copy of the proto-oncogene can drive the cell toward cancer
71
Q

tumorigenesis - recessive mutation

A
  • tumor suppressor genes (APC and p53)
  • loss of function mutations
  • both copies of the genes must be lost to drive the cell toward cancer
72
Q

tumorigenesis: explain the paths to oncogenic mutations

A
  • mutation in coding sequence
  • gene amplification
  • chromosome rearrangement
73
Q

tumorigenesis: paths to oncogenic mutations - mutation in coding sequence

A

results in hyperactive protein made in normal amounts

74
Q

tumorigenesis: paths to oncogenic mutations - gene amplification

A

results in a normal protein that is overproduced

75
Q

tumorigenesis: paths to oncogenic mutations - chromosome rearrangement

A
  • 2 results:
    1. nearby regulatory DNA sequence causes normal protein to be overproduced
    2. fusion to actively transcribed gene produces hyperactive fusion protein
76
Q

tumorigenesis - how can a tumor suppressor gene be eliminated

A
  • whole parental chromosome is lost
  • region containing the normal gene is deleted
  • loss of function mutation is in the parental gene
  • gene activity is silenced by epigenetic changes
77
Q

what are alterations that will result in a cancer cell

A
  1. alterations in cell proliferation
  2. alterations in DNA damage response
  3. alterations in cell growth

Cell Bio (21 decks)

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