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Life Protection > Cell Cycle > Flashcards

Cell Cycle Flashcards

1
Q

What is the cell cycle?

A

functional process that a cell goes through until it has divided into 2 genetically identical daughter cells

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2
Q

What are the main functions of the cell cycle?

A
  • replace lost body cells (sloughing of GI epithelia, wound healing, inflammatory response)
  • replaced old cells
    (old RBCs, destruction in spleen)
  • undergo clonal expansion (lymphocytosis in infection)
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3
Q

What are the 2 main stages of the eukaryotic cell cycle?

A
  • interphase

- mitosis (M phase)

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4
Q

What are the sub-phases of interphase?

A

G1, S, G2

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5
Q

What are the stages of mitosis?

A 
PMAT-C
prophase
(pro)metaphase
metaphase
anaphase
telophase

cytokinesis

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6
Q

Which cells CAN enter the cell cycle?

A

Cells with:

  • HIGH MITOTIC ACTIVITY
  • that divide upon appropriate stimulation
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7
Q

Which cells CANNOT enter the cell cycle?

A

post-mitotic cells = terminally differentiated

these are usually highly specialised cells, which are permanently arrested from cell cycle (senescent)

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8
Q

What are the 3 main types of cells that CAN enter the cell cycle?

A
  • labile
  • quiescent (stable)
    [ - permanent ]
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9
Q

What are labile cells?

A

rapidly divide with short G1 phase
never in G0 phase
“rapidly dividing” cells (most affected in chemo

e.g. skin, epithelia haematopoetic tissue

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10
Q

What are quiescent/stable cells?

A

Leave G0 phase when stimulated (e.g. damage)
Enter into G1 phase from G0

e.g. hepatocytes, perioseal cells, lymphocytes

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11
Q

What are permanent cells?

A

remain in G0 phase
Can only be replaced by stem cells

e.g. skeletal muscle cells (stem cells = satellite cells), neurons, RBCs

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12
Q

What is the G1 phase of interphase in cell cycle?

A
  • starting point in cell cycle
  • longest phase
  • one of the gap phases (M-> S phase)
  • stimulus required for entry from G0 phase
  • phase where cell prepares for S phase
  • move on when cell is properly prepared for S phase
  • if not, cell cycle is arrested at G1 phase
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13
Q

What is the S phase of interphase in cell cycle ?

A

DNA replication

  • occurs semi-conservatively
  • anti-sense strands used as template for new strand (sense) synthesis
  • Binding of complimentary bases via Chargaff’s rule
  • High replcation fidelity
  • will double DNA content at end of S phase
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14
Q

What mediates the high replication fidelity in S phase of cell cycle?

A
  • complimentary base pairing (GC, AT): incorrect pairing will cause unstable H-bond formation
  • proof reading DNA Pol activity
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15
Q

When does the cell progress from S phase to G2 phase?

A

when all chromosomes have been duplicated correctly (and checked for errors)

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16
Q

What is G2 phase?

A
  • shorter than G1 phase (usually)
  • preparation for mitosis
  • organelle synthesis (e.g. centrioles and mitotic spindle proteins)
  • driven by G2 regulatory proteins
  • any errors found will arrest the cells in this G2 phase
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17
Q

When do cells progress from G2 phase to M phase?

A

All in order for M-phase

correct organelles, DNA proofread and checked for errors etc

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18
Q

What is M phase?

A

= mitotic phase

- MITOSIS + CYTOKINESIS

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19
Q

What is mitosis?

A

= PMAT

- division of nucleus

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20
Q

What is cytokinesis?

A

final stage of cell cycle

physical division of cytoplasm and organelles

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21
Q

What occurs in prophase?

A
  • condensation of chromosomes
  • centrosomes move to opposite poles
  • mitotic spindle forms
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22
Q

What occurs in PROmetaphase?

A
  • disintegration of nuclear envelope

- chromosomes attach to mitotic spindle

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23
Q

What occurs in metaphase?

A
  • centrosome are at opposite poles

- chromosomes line up at the equator

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24
Q

What happens at anaphase?

A
  • pairs of chromosomes separate with one chromosome moving to each pole (soon to be new cell)
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25
Q

What happens at telophase?

A
  • one chromosome from each original pair reaches at each pole
  • chromosomes decondense
  • nuclear envelope reforms
26
Q

What happens at cytokinesis?

A

division of cytoplasm into identical daughter cells

27
Q

What is meiosis?

A
  • production of 4 haploid cells
  • 2 processes of cell division (cytokinesis)
  • homologous recombination occurs
  • CHIASM structure allows DNA exchange between DNA inherited from mother and father
28
Q

What is mitosis?

A
  • production of 2 diploid cells
  • only one stage of cell division (cytokinesis)
  • no homologous recombination
  • therefore no DNA exchange between tightly linked chromosomes
29
Q

What happens at the end of M-phase?

A
  • some cells re-enter cell cycle at G1 and divide again (this continues until senescence - associated with loss of telomerase activity)
  • some cells become quiescent (e.g. via contact inhibition)
  • some cells exit G1 and enter G0 for specialisation (terminal differentiation)
30
Q

What is the function of cell cycle checkpoints?

A
  • correct errors detected prior to next phase
  • withdraw from cell cycle if major error detected
  • apoptosis may be stimulated if errors cannot be corrected
31
Q

Where are the 3 major checkpoints in the cell cycle?

A
  • G1/S checkpoint
  • G2/M checkpoint
  • M checkpoint
32
Q

What does the M-checkpoint control?

A
  • controls progression from metaphase to anaphase
33
Q

Which cytokine can stop cell progression at G1/S checkpoint?

A

TGF-beta

34
Q

Give an example of a trigger for arresting a cell at the M-chekpoint

A
  • if spindles are not correctly aligned in the central axis (equator) of cell
35
Q

What triggers are screened at the G1/S phase checkpoint?

A
  • cell size
  • nutrient and growth signals sufficient?
  • DNA damage?
36
Q

What triggers are screened at the G2/M phase checkpoint?

A
  • correct DNA replication

- DNA damage

37
Q

triggers are screened at the M phase checkpoint?

A
  • correct separation of chromatids

- centrally aligned mitotic spindle

38
Q

How can phosphorylation activate/inhibit a protein? What are the advantages of this modification type?

A
  • alter physical properties, causing conformational change
  • alter hydrophobicity or interactions
  • speedy process
  • does not need new protein synthesis to re-activate or inhibit (temporary modification)
  • reversible
39
Q

What are cyclins?

A
  • involved in cell cycle regulation

- tightly regulated abundance during cell cycle (specific to cell-cycle phase)

40
Q

What are the CDKs?

A

= cyclin dependent kinases

  • stable abundance throughout cell cycle
  • inactive until bound by cyclin
  • degradation/removal of bound cyclin will terminate Cdk activity
41
Q

What is the function of the cyclin-CDK complex?

A

phosphorylation of other target proteins to activate them

42
Q

How do cyclin-CDKs function in the up regulation of DNAPol by Rb?

A

Rb is usually sequestered in a complex with E2F (inactive)

At specific stages (G1), cyclin-CDK complex phosphorylates Rb

This causes Rb to dissociate from E2F. E2F then translocates to nucleus to up regulate DNAPol expression

43
Q

What is the retinoblastoma protein?

A

= Rb (tumour suppressor gene)

  • key cyclin-CDK target protein in G1 and G1/S checkpoint
  • regulation of DNAPol transcription
44
Q

What are CDKi proteins?

A

= inhibitors of cyclin-dependent kinases

45
Q

What are the 2 types of CDKi proteins?

A
  • Inhibitor of kinase 4 family (INK4)

- CDK Inhibitory Protein/Kinase Inhibitory Protein (CIP/KIP) family

46
Q

How do INK4 proteins work?

A

= CDKi proteins

e.g. p15 (INK4b)
expression is stimulated by TGF-beta
specifically

47
Q

How do CIP/KIP proteins work?

A

= CDKi proteins

e.g. p21 (Cip)
Expression stimulated WEAKLY by TGFb.

Expression STRONGLY stimulated by DNA damage (involves p53).

Inhibit all other CDK-cyclin complexes (late G1, G2 and M).

Are gradually sequestered by G1 CDKs thus allowing activation of later CDKs.

48
Q

What is the p53 protein?

A
  • activated in response to DNA damage

- Phospho-p53 is ACTIVE form (longer half life than inactive form)

49
Q

What is the main function of p53?

A

induced CDKi expression (e.g. p21)
causes cell cycle arrest (in G1)
until repair of DNA damage

50
Q

What happens if DNA damage cannot be repaired when the cell cycle is arrested?

A

cell dies by apoptosis

[important function of tumour suppressors)

51
Q

What is a mitogen?

A
  • cytokines which stimulate cell proliferation
  • bind to cell-surface receptors-> promote cell cycle initiation and proliferation
  • some mitogens are encoded by photo-oncogenes
52
Q

Give an example of a mitogen (implicated in breast cancer)

A

Her2
ER
PR

53
Q

What cell cycle mechanisms are dysfunctional in cancer cells?

A
  • ignore normal checkpoint signals
  • enter S phase even with genetic damage
  • unresponsive to contact inhibition
  • unresponsive to apoptotic cells
54
Q

What are the types of DNA damage?

A
  • mismatched bases
  • chemical modification of bases
  • bulky DNA adducts
  • dsDNA breaks
55
Q

Which drugs target the S-phase of the cell cycle?

A
  • 5-fluoro-uracil (5-FU)

- bromodeoxyuridine (BrdU)

56
Q

How does 5-FU work?

A

targets S-phase

- prevents synthesis of dTMP needed for DNA replication. Leads to apoptosis

57
Q

How does BrdU work?

A

targets S-phase

- used in research to identify active replicating cells by labelling of thymidine incorporated into new DNA

58
Q

Which drugs target the M-phase of the cell cycle?

A
  • colchisine
  • vinka alkloids
  • paclitaxel (taxol)
59
Q

How does colchicine work?

A

targets M-phase

- stabilises free tubular, arresting cell cycle and causing death

60
Q

How do Vinka alkaloids work?

A

block beta tubular polymerisation and so inhibit cell division

61
Q

How does Paclitaxel work?

A

targets M-phase

stabilises microtubules, preventing breakdown of polymerisation

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