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Biomed year 2 sem 1 > BMS2002 - cell cycle > Flashcards

BMS2002 - cell cycle Flashcards

1
Q

what needs to happen to carry out a cell cycle

A

chromosomes duplicated
other organelles copied
cells grow
chromosomes segregated correctly
cell physically divides

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2
Q

G1 phase

A

Gap 1
- decides if conditions are right for full cycle
- growing, prep for DNA synthesis

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3
Q

S phase

A

synthesis
- replicating DNA and centrosomes

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4
Q

G2 phase

A

Gap 2
- decide if conditions are right for mitosis

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5
Q

M phase

A

chromosome segregation and cytokinesis

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6
Q

G0 phase

A

resting state - cells not in the cell cycle
- terminally differentiated cells, quiescent cells, senescent cells

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7
Q

CDKs

A

Cyclin Dependent Kinases
- master regulators
- activated by cyclin proteins (influence substrate specificity)

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8
Q

APC/C

A

ubiquitin ligase
- ubiquitylation of M- cyclin to tag them for degregation

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9
Q

CKIs

A

CDK inhibitory proteins

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10
Q

SCF

A

ubiquitin ligase
- signals degradation of CKIs to promote G1-S transition

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11
Q

G1-S checkpoint

A
  • checks nutritional conditions
  • is cell recieving proliferation signals?
  • has DNA damage been repaired?
    once passed, cell is committed to entire cell cycle
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12
Q

G2-M checkpoint

A
  • has DNA damage been repaired?
  • is DNA replication complete?
  • is the cell big enough?
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13
Q

Metaphase-Anaphase checkpoint

A

spindle assembly checkpoint
- are chromosomes properly attached to spindle?
satisfied -> APC/C activated -> cyclin B degraded -> cells exit metaphase into anaphase

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14
Q

if checkpoint is not satisfied

A

cells withdraw from cycle
- senescence, allows cell to remain in tissue but not proliferate
apoptosis
- removes cell from organism

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15
Q

G1 CDKs and cyclins

A

CDK4 and 6
cyclin D

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16
Q

G1/S CDKs and cyclins

A

CDK2
cyclin E

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17
Q

S CDKs and cyclins

A

CDK2, CDK1 (CDC2)
cyclin A

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18
Q

G2/M CDKs and cyclins

A

CDK1 (CDC2)
cyclin B

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19
Q

4 ways cells control CDK-cylin kinase activity

A
  1. transcription
  2. CDK inhibitors - CKIs
  3. antagonized phsophorylation and dephosphorylation
  4. ubiquitin mediated proteolysis
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20
Q

early G1 genes that determine G1/S transition

A

Myc
- transcriptional factor
- can react to mitigens -> cyclin D
SCF ubiquitin ligase for protein proteolysis

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21
Q

where does DNA replication begin

A

at oriC
- recognised by ORC (origin recognition complex) for DNA unwinding
- multiple in euk
- can only be activated once per cycle to preserve genome integrity

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22
Q

formation of precipitation complex in vertebrates

A

geminin binds Cdt1 -> prevents loading MCM complex onto origin DNA

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23
Q

formation of precipitation complex in mitosis

A

APC/C degrades geminin -> ubiquitin proteolysis -> Cdt1 released -> ORC-CDC6-Cdt1 complex recruits MCM 2-7 complex on origin DNA

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24
Q

replication starts when..

A

CDK2-cyclinA phosporylates MCM2-7 -> forms CMG helicase with GINS complex and CDC45

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25
Q

Helicase in DNA rep initiation

A

breaks h-bonds -> unwinding -> DNA replication bubble and replication forks

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26
Q

SSBPs and RPA

A

Single stranded binding proteins
Replication protein A
- bind to unwound strands -> stabilises and prevents base pairing

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27
Q

type IIA topomerase

A

DNA relacation at the front of the replication fork in eukaryotes

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28
Q

gyrase

A

DNA relacation at the front of the replication fork in prokaryotes

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29
Q

RNA primase

A

during elongation:
uses ribose NTPs as a nucleotide source -> produce a short RNA primer -> provides attachment to original DNA template

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30
Q

DNA polymerase delta/III

A

adds dNTPs to 3’ end
- continuous synthesis on leading strand
- discontinuous synthesis on lagging strand -> okasaki fragments that need to be joined by DNA ligase
have endonuclease activity -> can proof read sequence and correct it

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31
Q

DNA sliding clamp

A
  • scaffold, keeps polymerase attached
  • processivity-promoting factor in DNA replication
32
Q

telomeres

A

form T-loop in eukaryotes -> prevents genes from being deleted
- shortened with each division, division will stop once at a critical length

33
Q

Hayflick limit

A

number of times a normal cell can divide before cell division stops
- doesnt apply to stem cells bc of telomerase activity in germ cells/ adult stem cells

34
Q

DNA damaging agents

A
  • DNA replication stress
  • polyaromatic hydrocarbons
  • UV light
  • oxygen radicals
  • ionizing radiation
  • chemotherapeutic reagents
35
Q

DNA damage types

A
  • base mismatch, insertion, deletion
  • single strand breaksm base oxidation
  • DNA adducts oyramidine dimers
  • intrastrand crosslinks
  • double strand breaks
36
Q

DNA repair mechanisms

A

MMR = mismatch repair
BER = base exclusion repair
NHEJ = non-homologous end joining
NER = nucleotide excision repair
HR = homologous recombination repair

37
Q

consequenses of DNA damage

A

transient cell cycle arrests
apoptosis
cancer
aging
inborn disease

38
Q

cells that never divide

A

mature muscle cells (e.g. cardiac muscle), nerve cells

39
Q

cells arrested in G0 but can resume proliferation

A

skin fibroblasts, smooth muscle cells, blood vessel endothelial cells, epithelial cells in liver/pancreas/kidney/lung/prostate/breast

40
Q

stem cells that need continuous cell renewal

A

blood cells, intestinal epithelial cells

41
Q

6 sages of mitosis

A

Prophase
Prometaphase
Metaphase
Anaphase
Telophase
Cytokinesis

42
Q

which cyclin drives entry into prophase

A

M-CDK - cyclinB-CDK1
- directly phosphorylates key substrate proteins
- regulates downstream mitotic kinases to phosphorylate additional substrates

43
Q

prophase - kinteochore assembly

A

M-CDK (cyclin B- CDK1) and aurora B kinases recruit kintochores

44
Q

kinetochore

A

microtubule binding site on chromosome, large macromolecular complex that assembles on the centromere

45
Q

prophase - chromosomes condense

A

cohesin is removed
condensins I and II co-operate to condense the chromosomes

46
Q

what happens during prophase?

A
  • interphase chromosome structure is lost
  • chromosomes condense
  • kinetochore assembly begins
  • microtubule dynamics change -> spindle starts to form
47
Q

what happens during prometaphase

A
  • nuclear envelope breaks down -> microtubules can access chromosomes
  • spindle assembles
  • microtubules attach to chromosomes
  • MAPs and motor proteins become active -> chromosomes can be moved on the spindle
48
Q

Microtubule structural properties

A
  • nucleated at minus end
  • dynamically unstable at plus end -> can grow and shrink from plus end
49
Q

MAPs

A

Microtubule Adapter Proteins
- allow cell components to bind microtubules
- modulate stability of microtubules e.g. NDC80/Nuf2 at kinetochores

50
Q

Spindle motor proteins

A
  • allow cell components to move along microtubules
    e.g. kinesin-5 (walks to plus end using ATP), Dynein (walks to minus end)
  • can carry various cargo proteins
51
Q

mitotic spindle assembly

A
  • nucleation of microtubules at centrosome (minus end)
  • formation of interpolar microtubules -> sliding moves centrosome apart
  • nuclear envelope breakdown -> microtubules can capture kinteochores
52
Q

processes in chromosomes bi-orienting on the spindle

A
  • making correct attatchment + error correction
  • spindle checkpoint - check attachments are corrrect
  • means of attachment changes once kinetochore reaches the plus end
  • end-on attachments require Ndc90-Nuf2 complex
53
Q

kinase Aurora B

A

detects bi-orientation
- localises to centromeres
- detects tension
- phosphorylates Ndc80 to remove microtubules from kinteochores

54
Q

metaphase

A
  • all chromosomes have bi-orientated + no unattached kinteochores remain
  • spindle checkpoint stops singnalling -> APC/C activated
  • M cyclin degraded -> exit from mitosis
  • securin is degraded to separase -> separates sister chromatids
55
Q

spindle checkpoint

A

chromosomes not properly attached -> error correction produces unattached kinetochores (detected by spindle)
unattached kinetochores -> MCC (mitotic checkpoint complex) -> inhibits APC/C -> prevents M-cyclin (CyclinB) degredation -> cells stay in mitosis

56
Q

Anaphase A

A

chromosomes move towards spindle poles
- driven largely by microtubule/kinteochore shrinking at plus end

57
Q

Anaphase B

A

spindle poles move apart
- driven largely by microtubule motors (E.g. kinesin-5, dynein)

58
Q

telophase

A
  • nuclear envelope refroms, nuclear pores inserted
  • chromosomes decondense
    condensins disassociate, cohesins re-associate
    -> enables formation of chromome looping structures for gene expression
59
Q

cytokinesis

A
  • contractile ring (Actin and myosin) -> cleavage furrow formation -> pinching of the dividing cell into two
60
Q

Cancer - when cell can’t exit the cycle

A
  • cell keeps dividing even if rejected at checkpoints
  • forced into the cell cycle
61
Q

mutated protooncogenes

A

become oncogenes
-> mimic a stuck accelerator
-> excessive growth and division

62
Q

2 tumour supressors

A

p53 - DNA damage response
Rb (retinoblastoma protein) - stop cell cycle entry (E2F transcription pathway)

63
Q

CIN (chromosomal instabilities) in cancer

A
  • generation of abnormal chromosome numbers (aneuploidy) due to chromosome mis-segregation
  • chromosome rearrangements (translocations) due to abberant repair of DSB - fusion of wrong ends
64
Q

Causes of aneuploidy in mitosis

A
  • inappropriate kinetochore-MT attachments
  • compromised SAC
  • centrosome overduplication (cancer and microcephaly)
  • problems with chromosome cohesion
  • cytokinesis failure, cell fusion, endoreduplication (too many times through interphase) -> tetraploidy 4n
65
Q

aneuploidy at a cellular level ->

A

substantial fitness loss
- impaired proliferation
- metabilic alterations
- defective stress response

66
Q

Cancer’s mechanisms to tolerate aneuploidy

A
  • lowering DNA damage response (p53)
  • mistakes in cell division -> p53 activation -> increases cancer cell’s tolerance to insult inculding CIN
  • increasing stress tolerance
  • prolonged mitosis (SAC)
67
Q

Aneuploidies that benefit tumorigenesis

A
  • trisomy Ch12 -> increased proliferation and tumorigenesy of hESC
  • in colorectal cancer: single trisomies -> advantage and increased tumorigenic behaviour upon stress
68
Q

ABL

A
  • tyrosine kinase that becomes over activates due to reciprocal translocation
69
Q

ABL protooncogene activation

A

operates in the G1-S transition in response o mitogens

70
Q

agents that promote DSB

A

DNA topomerase II poisons
Radiation
CIN

71
Q

what causes chromosome translocations

A

arise from abberant DSB repair in interphase

72
Q

what guides DSB misrepair

A
  • sequence homology at chromosome breakpoint
  • 3D chromosomal organisation in interphase
73
Q

ABL kinase is activated by…

A

chromosome translocation
- releases SH3 SH2 internal inhibition
- becomes cytoplasmic
- promotes oligomerization and autophorphorylation

74
Q

chromosome rearrangements ->

A

gene fusion -> hybrid/chimeric gene targeting transcription factors and tyrosine kinase

75
Q

Rb

A

retinoblastoma protein - first tumour suppressor identified
- operates at G1-S transition
- loss of Rb function from mutation -> retinal tumours in children
- Rb inactivation -> predisposition to cancer

76
Q

Retinoblastoma

A

rare childhood eye tumour that arises in precursors to photoreceptor cells
- Rb loss
- sporadic (no fam history): unilateral, no increased risk of other cancers
- familial: bilateral, high risk of other cancers

Biomed year 2 sem 1 (7 decks)

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