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BIOC2301 > Health and Disease: Cell Cycle Prof. Blair > Flashcards

Health and Disease: Cell Cycle Prof. Blair Flashcards

1
Q

Give the phases of interphase?

A

G1, S and G2. Also G0 but this is newly found and still being researched.

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2
Q

Describe G1?

A

Major variable length phase for cell growth and expansion. Approximately 9 hours long.

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3
Q

What happens when cells become quiescent?

A

They get locked in G1 phase.

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4
Q

How long is S phase?

A

Approximately 10 hours.

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5
Q

Describe G2 phases?

A

For preparation for mitosis, approximately 4-5 hours long.

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6
Q

What is cytokinesis?

A

The contractile ring separating daughter cells at the end of telophase.

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7
Q

What does cell viability and integrity depend on?

A

Accurate duplication and segregation. The genome must be correctly copied once and divided equally between the daughter cells.

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8
Q

What is mitosis?

A

All phases except for interphase, it lasts approximately 30 minutes.

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9
Q

What routes can cells take?

A

Grow and divide (possible proliferation), differentiation, death (apoptosis), rest (possible quiescence).

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10
Q

What methods can be used to study the mammalian cell cycle?

A

Cell synchronisation using reversible inhibitors, DNA synthesis using bromodeoxyuridine and anti-BUdR antibodies, DNA content using flow cytometry (FACS), plant detect S-phase cell with pulse labelling and nucleotide analogue BrdU.

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11
Q

How is cell synchronisation using reversible inhibitors used to study the mammalian cell cycle?

A

Colcemid binds microtubules- inhibits M phase by freezing the microtubules, reversible inhibitor, thymidine or hydroxyurea inhibit DNA replication in S phase when in high concentrations.

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12
Q

What is the disadvantage with studying mammalian cells using cell synchronisation using reversible inhibitors?

A

No method to block in G1 or G2 phase.

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13
Q

How can FACS, DNA content measurement using flow cytometry, be used to study the cell cycle in mammalian cells?

A

Use a graph which can have a program fitted to identify stages and use different reagents to ID etify different things.

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14
Q

What is the disadvantages with studying mammalian cell cycle with plant detect S-phase cell with pulse labelling and nucleotide analogue BrdU?

A

Shows very few cells in mitosis.

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15
Q

Name the main steps of the cell cycle?

A

Interphase, prophase (early then late), metaphase, anaphase, telophase (and cytokinesis).

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16
Q

What are some systems to study the cell cycle?

A

Cell fusion between cells in different stages of the cycle (uses polyethylene glycol to fuse plasma membranes)
Frog and amphibian eggs and embryos (Led to discovery of maturation or mitosis promoting factor or MPF)
Fission and budding yeast (Led to discovery of cell division control or cdc genes)

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17
Q

What are CDC genes?

A

Cell division cycle genes, they code for which regulate cell cycle events.

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18
Q

What is MPF?

A

Mitosis-promoting factor, a heterodimer made of 1 molecule of cyclin B and 1 molecule of cdc2

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19
Q

What is cdc2?

A

Cell division cycle gene 2 which is a cyclic dependent kinase aka. cdk

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20
Q

What proteins are involved in regulating the G2/M transition in mammalian cells?

A

cdc2, cyclin B (a subunit associated with cdc2 kinase), cdc25C (a protein phosphatase), wee1 (a protein kinase which makes cells small), CAK (cdk-activating kinase).

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21
Q

How do cdc2 levels change throughout the cell cycle?

A

Remain at a constant high level throughout.

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22
Q

How do cyclin B levels change throughout the cell cycle?

A

Gradually increases after S phase and plummets in M phase.

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23
Q

How do MPF levels change throughout the cell cycle?

A

Shoots up after G2 before M phase and then plummets in M phase.

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24
Q

What are the sites of cdc2 phosphorylation?

A

One near the N-terminus which wee1 phosphorylates and one in the centre which CAK phosphorylates.

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25
What do both cdc2 phosphorylation sites depend on?
Cyclin-bound cdc2.
26
How is cdc2 differentially phosphorylated during the cell cycle?
G2: cdc2 is in complex with cycB, wee1 and CAK, both sites are phosphorylated but the product is inactive. (Once phosphorylated wee1 and CAK leave). M phase: cdc25 binds and removes the N-terminal phosphate replacing it with a tyrosine-15, this activates cdc2. G1: cycB is released and the central phosphate removed and replaced with threonine-16, this inactivates cdc2.
27
How do CAK, wee1 and cdc25 levels change throughout differential phosphorylation?
CAK remains at a high levels. wee1 is high throughout G1, S and G2 and plummets in at the end of G2 and shoots back up during M. cdc25 is low throughout G1, S and G2 and then shoots up after G2 and falls during- opposite to wee1.
28
Why is cdc2 activated in this way?
Allows for rapid switching and is brought about by positive and negative feedback.
29
What cdk/cyclin are required for G2-M transition?
cdk1/cyclin B
30
What cdk/cyclin are required for G1?
cdk4/ cyclin D
31
What cdk/cyclin are required for G1-S transition?
cdk2/ cyclin E
32
What cdk/cyclin are required for S?
cdk2/cyclin A
33
What is the APC?
Anaphase promoter complex: targets cyclin B for degradation by proteolysis after metaphase/anaphase.
34
How does the APC work?
Contains a ubiquitin ligase which degrades the protein (securin) which links sister chromatids.
35
Describe the G1-S checkpoint?
Negatively regulated by hypophosphorylated Rb (recruits histone deacetylase, HDAC; leads to transcriptional repression). E2F is a transcription factor that activates transcription of S phase genes (coding for proteins involved in DNA synthesis), cyclin E and its own expression
36
What is Rb?
Rb is a tumour suppressor, mutated/deleted in retinoblastoma.
37
What are CDKI?
Cyclin-dependent Kinase Inhibitors: they regulate cdk activities and arrest the cell cycle in response to such anti proliferative signals as contact with cells, DNA damage, terminal differentiation and senescence.
38
Describe CDKI?
Two major families: CIP (CDK inhibitory proteins) e.g. p21, p27 and p57 and INK (Inhibitor of cdk4) e.g. p16 May act as S phase inhibitors, degraded by proteolysis in late G1.
39
Describe the action of p21?
P21 transcription activated by p53 in the DNA damage response – arrests cycle in G.
40
At what points do CDKI check?
Before M phase for un replicated or damaged DNA, before G1 for chromosome misalignment, before S for damaged DNA.
41
Describe the DNA damage response?
Protein kinase ATM phosphorylates p53. Phosphorylation blocks binding by MDM2, a ubiquitin ligase that targets p53 for proteolysis P53 activates p21 transcription, inhibits cdk-cyclin complexes, arrests cells in late G1 - allows damage to be repaired. ATM also activates Chk2, a protein kinase involved in mitotic checkpoint control, inhibiting entry to M phase.
42
What is p53?
P53 is a transcription factor (53kDa), frequently lost/mutated in multiple cancers.
43
When are increased levels of p53 found?
In irradiated cells.
44
What cellular process do very high levels of p53 activate?
Apoptosis- programmed cell death.
45
What is the opposite of apoptosis?
Necrosis- death following injury, infection or trauma.
46
What are some markers for apoptosis?
Cell morphology, DNA ladders, TUNEL assay (Labelling of termini of DNA fragments with fluorescent groups by the enzyme terminal transferase), Binding of Annexin V (labelled with a fluorescent dye, FITC) to cells, Caused by membrane changes, Activation of caspase enzymes.
47
What are the three states of apoptosis?
Decision, execution and death.
48
How is apoptosis controlled?
Extracellularly by signalling from death receptors on the cell surface. Intracellularly by dsDNA breaks, p53, UV radiation, hypoxia and withdrawal of growth factors.
49
What are caspases?
Cys-catalysed aspartate targeting proteases. All have similar substrate specificities and amino acid sequences and induce apoptosis. Firstly expressed as pro-enzymes which require activation. Contain 3 domains: N-terminal for activation regulation, small and large domain.
50
What is the only caspase that doesn't induce apoptosis?
Interleukin converting enzymes (ICE)
51
How are caspases activated?
By proteolytic cleavage between domains. The large and small domains form heterodimers with an activation site in between.
52
How do caspases work?
Thought a caspase cascade. Initiator caspases activate a cascade resulting in activation of executioner caspases.
53
How do caspase inhibitors inhibit apoptosis?
Bind to the catalytic site of the catalase inhibiting the initiator caspases activating the executioner caspases. Eg. c-FLIP
54
Describe the extrinsic pathway of apoptosis?
1) Fas ligand on the killer lymphocyte binds to the Fas death receptors on the target cells. 2) FADD adaptive protein is recruited with its death domain and death effector domain and the procaspase (8 or 10) is also recruited with its death receptors in the assembly of DISC. 3) Procaspase is activated and cleaved. 4) Activation of executioner caspases then cause apoptosis.
55
What are death receptors?
Membrane bound receptors which signal death by binding cytotoxic ligands.
56
What mechanism exist to prevent external death signals?
Soluble decoy receptors, membrane bound decoy receptors and intracellular signalling activators and inhibitors.
57
How are death receptors activated?
Ligand binding followed by receptor trimeristaion (into a homotrimer), intracellular death domain cluster signals (pro-apoptotic signal).
58
Describe the intrinsic pathway of apoptosis?
1) Apoptotic stimulus acts on mitochondrion. 2) Cytochrome C in intermembrane space are released. 3) Apaf1 (apoptotic protease activating factor 1) is activated and hydrolysis of dATP to dADP. 4) Apoptosome assembles by the clustering of the caspase recruitment domain. 5) Procaspase 9 is recruited and activated which activates executioner procaspases.
59
Describe the Bcl-2 family?
Anti-apoptotic, found in B Cell Lymphomas. 25-26kDa membrane protein associated with membranes, mitochondria. Homologues of Bcl-2 e.g. Bax, pro-apoptotic, forms heterodimers with Bcl-2 and inactivates Bcl-2. Some viruses contain Bcl-2 homologues e.g. adenovirus E1B-19kDa protein
60
Name the 3 classes in the Bcl-2 family?
Anti-apoptotic Bcl-2 protein, pro-apoptotic BH123 protein, pro-apoptotic BH3-only protein.
61
Describe the intrinsic pathway involving BH123 proteins?
Apoptotic stimulus activates BH123 protein, BH123 proteins aggregate and cytochrome c and other intermembrane space proteins are released.
62
What does anti-apoptotic Bcl-2 protein do?
Inhibits aggregation of BH123 proteins.
63
What does BH3-only protein do to Bcl-2?
It stops Bcl-2 from blocking aggregation.
64
What are telomeres?
The termini of the eukaryotic linear chromosomes.
65
What is the structure of telomeres?
Human telomeres contain thousands of repeats of the six nucleotide sequence TTAGGG (tetrahymena have repeats of GGGGTT). Human telomerice repeats extend for up to 12kb. Most of the telomeric DNA is double-stranded with a G-rich single stranded 3'-terminal overhang. Non-coding DNA.
66
What are the functions of telomeres?
Protect the chromosome ends from shortening, prevent chromosomes ends becoming entangles and adhering to eachother, they assist in the paring of homologous chromosomes during prophase of meiosis 1.
67
What happens to telomeres during mitosis?
Approximately 100 bp is lost.
68
What synthesises telomeres?
Telomerase
69
What is telomerase?
A ribonucleoprotein complex which is involved in synthesis of DNA of telomeres in many organisms, contains a protein component with enzymatic activity of a specialised reverse transcriptase termed TERT (telomerase reverse transcriptase) and a TERC (Telomerase RNA component) which provides the template to guide the insertion of the repeat.
70
Where is telomerase generally only found?
Germline cells, certain adult stem cells and progenitor cells, cancer cells and unicellular eukaryotes.
71
What are telomeres related to?
Cancer (failure to prevent cell division) and ageing.

BIOC2301 (15 decks)

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