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Phase 1 > The Cell Cyle and Signalling > Flashcards

The Cell Cyle and Signalling Flashcards

1
Q

what is the definition of the cell cycle?

A

the interval between 2 successive mitosis divisions resulting in the production of 2 daughter cells with identical chromosomes

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2
Q

what are the 4 main phases of the cell cycle?

A

G1, S, G2 and M

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3
Q

what stages of the cell cycle make up interphase?

A

G1, S and G2

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4
Q

what is G0? how do cells exit G0?

A
  • cells are no actively dividing -> quiescence

* external signal (eg. APC) or mitogenic factor

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5
Q

describe G1 (4)

A

1 - cells enter G1 after stimulation by a growth factor
2 - RNA and proteins are synthesised in preparation for S phase
3 - growth in size
4 - restriction point, after which the cell is committed to division

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6
Q

describe S phase (2)

A

1 - DNA is synthesised to make 2 copies of chromosome

2 - intra-S checkpoint with p53 which checks for DNA defects

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7
Q

describe G2 (2)

A

1 - organelles replicated in preparation for mitosis

2 - further growth (double in size since start of G1)

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8
Q

describe prophase (4)

A

1 - chromatin condenses
2 - nucleolus + nuclear membrane disappear
3 - centrosomes move to opposite poles
4 - chromosomes attach to microtubules

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9
Q

describe metaphase (1)

A

1 - spindle fibres align chromosomes along middle of nucleus

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10
Q

describe anaphase (2)

A

1 - proteolytic cleavage of centromere

2 - sister chromatids separate and move to opposite sides of the cell

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11
Q

describe telophase (3)

A

1 - new membranes form around daughter nuclei
2 - chromosomes condense
3 - spindle fibres disperse

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12
Q

what group of proteins regulate progression through the cell cycle? what action do they perform?

A
  • cyclin-dependent kinases

* phosphorylate serine and threonine amino acids on target proteins

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13
Q

what are cyclins?

A

small activator proteins whose concentration varies throughout the cell cycle (constantly synthesised and broken down)

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14
Q

describe how CDK1 (aka Maturation Promoting Factor) is activated (5)

A

1 - cyclin B is transcribed and accumulates during G1
2 - when a threshold amount is reached, CDK1 proteins are activated
3 - inactive CDK1 loses its net phosphorylation to form a complex with cyclin B
4 - permits the cell to enter mitosis
5 - cyclin B is degraded to prevent further CDK activity

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15
Q

what are the 2 ways that CKIs work?

A
  • CDK inhibitor
  • inactivate CDK-cyclin complex
  • act as competitive inhibitor
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16
Q

what actions does active CDK1 perform to start mitosis? (3)

A
  • phosphorylates nuclear lamins (n.envelope disassembles)
  • phosphorylates condensins + histones causing chromosome condensation
  • phosphorylates microtubule-associated proteins to allow spindle formation
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17
Q

what conditions are monitored by the cell to regulate the cell cycle?

A
  • favourable external environment - presence of growth factor
  • favourable internal environment - sufficient cell growth
  • DNA damage
  • replication errors
  • spindle attachment
  • chromosome integrity
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18
Q

where in the cell cycle is the restriction point? what conditions does it check for?

A
  • end of G1

* cell size + favourable external conditions with growth factor

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19
Q

describe how a cell passes the restriction point (5)

A

1 - retinoblastoma (Rb) inhibits the transcription factor E2F, therefore preventing proteins required for S phase from being synthesised
2 - growth factor is detected on cell surface -> Rays signalling pathway
3 - cyclin D synthesised and accumulates, complexes with CDK 4 and 6 forming activated kinases
4 - Rb is phosphorylated, therefore E2F is uninhibited
5 - S phase proteins synthesised allowing cycle to continue

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20
Q

where are the 2 DNA damage checkpoints in the cell cycle? why are each of them important?

A
  • late G1: check DNA before it is replicated

* G2: check DNA before it is passed to daughter cells

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21
Q

what are 3 causes of DNA damage?

A
  • chemical mutagens
  • radiation
  • replication errors
22
Q

what molecule detects DNA damage at checkpoints?

A

p53

23
Q

what actions does p53 perform to stop a cell’s progression through the cell cycle? (3)

A
  • signals production of p21 - a CKI to inhibit CDK-cyclin complexes for the next phase (either S or M)
  • halts cell cycle to allow for DNA repair (low cellular stress)
  • promotes apoptosis (high cellular stress)
24
Q

what happens at the spindle checkpoint in the cell cycle?

A

anaphase promoting complex is inhibited until all chromosomes are attached to spindle

25
Q

what are proto-oncogenes? (2)

A
  • encode proteins involved in regulation of cell growth and mutation
  • when mutated, proto-oncogenes become oncogenes which are always active and initiate / speed up proliferation
26
Q

what are 3 types of oncogenes? give examples of each

A
  • cell surface receptors: amplify signals (HER2)
  • transducers: activate enzyme cascades inappropriately (Ki-Ras)
  • protein synthesis: accumulation of cell cycle regulators (cyclin D amplification)
27
Q

what 4 types of mutation can lead to a proto-oncogene to become an oncogene? what effect does each of the mutations have on the protein?

A
  • deletion / point mutations - hyperactive protein made in normal amounts
  • regulatory mutation - normal protein is overproduced
  • gene amplification - greatly overproduced
  • chromosome rearrangement - hyperactivity or overproduction
28
Q

what is the role of tumour suppressors?

A
  • maintain integrity of the genome
  • cause cell cycle arrest in abnormally dividing cells
  • or repair DNA damage
29
Q

give 3 examples of tumour suppressors

A
  • Rb - blocks entry to cell cycle
  • p53 - detects DNA damage to haunt cell cycle
  • BRACA1 - repaired DNA (mutated in may types of breast and ovarian cancers)
30
Q

why are most tumour suppressors described as requiring ‘two hits’? what important tumour suppressor does this not apply to?

A
  • both alleles of the protein must be mutated for the protein to be inhibited as a tumour suppressor
  • p53 is made up of 4 polypeptide chains, ie. shape of overall protein will mostly be affected even if only one allele is mutated
31
Q

what are the 3 broad signal types in the body?

A
  • physical - response to sensation
  • electrical - impulses
  • chemical - hormones, growth factors, neurotransmitters
32
Q

what are the 4 types of hormones based on chemical structure? give examples of each

A
  • amine - amino acids with a modified group (noradrenaline)
  • peptide - short amino acid chains (oxytocin)
  • protein - long peptide chains (human growth hormone)
  • steroid - derived from lipid cholesterol (oestrogen, testosterone)
33
Q

what are the 4 ranges of action for hormones?

A
  • endocrine - long distance, via blood
  • paracrine - short distance, via diffusion
  • juxtacrine - neighbouring cells, via cell:cell contact
  • autocrine - same cell
34
Q

describe how hydrophobic signals work (4)

A

(eg. steroid hormones)
1 - diffuse through phospholipid membrane
2 - bind to intracellular receptors
3 - hormone-receptor complex acts as a transcription factor
4 - binds to DNA to alter gene expression

35
Q

what are 3 types of cell surface receptors? give examples of chemicals using these receptors

A
  • ion channel linked - ions flow into cell to change charge (glutamate neurotransmitter)
  • G-protein coupled (GPCR) - signal activates a G-protein which passes the signal into the cell (adrenaline)
  • enzyme linked - either via dimerisation or through direct activation of enzyme (receptor tyrosine kinases - growth factors)
36
Q

what is the definition of transduction?

A

relay system that takes signal to a specific place to trigger a specific response, may also amplify signals

37
Q

what are the 2 main types of transduction

A
  • enzyme cascade

* secondary messengers

38
Q

what type of transduction is the MAPK/Ras pathway? describe the MAPK/Ras pathway - activation order (6)

A

• enzyme cascade

1 - EGF binds to and activates the tyrosine kinase receptor EGFR
2 - active EGFR activates SOS
3 - SOS activates K-Ras
4 - K-Ras activates MAP3K
5 - MAP3K activates MAP2K, which activates MAPK (amplification step)
6 - MAPK activates Myc, a transcription factor that synthesises proteins in response to the signal

39
Q

what is the basic principal of secondary messengers?

A

small proteins produced in large quantities after receptor activation which then go on to actives several different proteins

40
Q

what is the structure of a G-protein coupled receptor?

A

7-span transmembrane structure

41
Q

what are 3 important signalling molecules that use GPCRs?

A

adrenaline, rhodopsin, glutamate

42
Q

what are the subunits of a G protein?

A

alpha, beta and gamma

42
Q

describe how a G protein is activated by an activated GPCR (4)

A

1 - G protein binds to activated receptor
2 - receptor promotes exchange of GDP for GTP (inactive to active state)
3 - when activated, G protein separates into 2 effectors - alpha unit + GTP and beta + gamma
4 - signal turned off by GAP/RGS -> cause GTP to hydrolyse and return G to heterotrimeric state

43
Q

describe the signalling pathway of adrenaline in increased blood glucose (6)

A

1 - adrenaline activates GPCR
2 - triggers activation of G protein -> alpha unit activation
3 - alpha unit activates adenylyl cyclase which produces the secondary messenger cAMP
4 - cAMP activates Protein Kinase A (PKA)
5 - PKA has 2 actions:
• phosphorylate and activate phosphorylase kinase
• phosphorylate and inhibit glycogen synthase
6 - phosphorylase catalyses glycogen to glucose, synthase is prevented from catalysing glucose to glycogen (glucose release)

44
Q

describe how the adrenaline signal is switched off (3)

A

1 - adrenaline detaches and GPCR inactivates
2 - G protein inactivated so cAMP production is inhibited
3 - phosphodiesterases breakdown remaining cAMP

45
Q

what are the effects that adrenaline produces in different tissues (5)

A
  • cardiac muscle: increase heart rate and force
  • airway smooth muscle: bronchodilation
  • BV of skeletal muscle: vasodilation
  • BV of peripheral organs: vasoconstriction
  • adipose tissue + liver: glycogenolysis
46
Q

what are the 4 ways that tissue specificity can be achieved for a single signalling molecule?

A
  • different GPCR to trigger different effects
  • different G protein
  • different effectors / trigger different events in effector
  • different secondary messengers that have different targets
47
Q

what are the 2 ways that an action potential can be started?

A
  • stimuli activates Na+ channels directly

* neurotransmitters binds to receptor and causes ion movement to trigger action potential

48
Q

what is summation? where does it occur in the axon?

A
  • both excitatory and inhibitory inputs are added together -> if the threshold potential is reached after adding together, then AP is triggered
  • axon hillock (beginning of axon just after cell body)
49
Q

what is the different between spatial and temporal summation?

A
  • spatial summation - inputs arise from different dendrites

* temporal summation - not enough time to reach resting potential between inputs (excitatory)

50
Q

what are the main chemical types of neurotransmitters? give examples (4)

A
  • amino acids + derivatives: glutamate (main excitatory in CNS), GABA (main inhibitory in CNS)
  • catecholamines (monoamines) derived from tyrosine: dopamine and serotonin
  • acetylcholine derived from choline (important at neuromuscular junction)
  • peptides: substance P and endorphins

Phase 1 (14 decks)

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