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biol2200 end of sem > Module 5 second half > Flashcards

Module 5 second half Flashcards

1
Q

cdc 2

A

cyclin dependent kinase (CDK)

Cdc 2+ = wild type = wee form

Cdc 2- = recessive = excess of wee1 or deficit of cdc25

Cdc 2D = deficit of wee1 (kinase inhibits mitosis) or excess of cdc25 (phosphatase - drives mitosis)

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2
Q

Kinase and phosphatase cascade

A

controls entry into mitosis

Wee 1 - phosphorylates Y15 of mitosis cdk, inactivating it
CAK - activated the Miro to f kinase by phosphorylation
Cdc25 - removes an inhibitory phosphate from mitotic cdk

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3
Q

Mitosis promoting factor (MPF)

A

mitotic cyclin/CDK

produced in G2 but kept phosphorylated (inhibited) until cell ready for mitosis

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4
Q

Checkpoints

A
  • points in cell cycle where cell can stop if something has gone wrong
  • driven by proteins that inhibit cell cycle progression
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5
Q

Mitotic checkpoint

A

DNA replication incomplete

ATR1 – CHK1 – (inactivates) – Cdc25

(ATR1 - checkpoint protein that is activated by single stranded DNA)

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6
Q

G2/M summary

A
  1. yeast mutants identified crucial players in G2/M transition, including activators and inhibitors of mitotic cyclin/CDK.
  2. phosphorylation of different CDK residues can inhibit and activate the mitotic cyclin/CDK.
  3. checkpoints ensure that cell has complete one ask before initiating the next. they target the major regulators of the cell cycle
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7
Q

Mitotic cyclin/CDKs and nuclear envelope

A
  • nuclear lamina support nuclear envelope
  • lamins A,B and C form lamina structure
  • mitotic cyclin/CDKs phosphorylate the lamin proteins, causing meshwork to breakdown
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8
Q

APC/C ubiquitin-protein ligase

A

ubiquitinates mitotic proteins at key stages of mitosis
1. induces anaphase - metaphase-anaphase transition
2. induce late steps in mitosis (late anaphase) (along with Cdc14)

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9
Q

Phosphatase PP2A

A

associated with centromeres and prevents cohesins near the centromere from being removed by phosphorylation - therefore they must be removed another way

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10
Q

Metaphase/anaphase transition

A

separation of chromatids

APC/C initiates this by inducing cohesin removal at the centromere.
(ring that surrounds chromosomes)
- cohesively keeps everything together (to remember)

  1. cohesins are composed of smc proteins and Scc1
  2. separase is a protease that cleaves Scc1
  3. securin binds separase, inhibiting it
  4. when all kinetochores bind MTs, Cdc20 binfd to APC/C
  5. APC/C polyubiquitinates (dooms) securin
  6. separase, uninhibited, cleaves Scc1
  7. chromaids are free to separate. this define anaphase
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11
Q

Degradation of mitotic cyclins

A

APC/C specificity changes late in anaphase once chromatids have separated

Cdc1 becomes active and leads the APC/C complex to the mitotic cyclin for degradation

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12
Q

Ubiquitination in G1-S phase transition

A

CKI binds to CDK/cyclin - inactive

SCF targets CKI and ubiquitinates it so then the CDK/cyclin is now active
- ready for S phase (?)

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13
Q

3 mechanisms of cell specification

A

cell to cell interactions
- cell beside you determines your fate

asymmetric
- identical inside but ones slightly larger

morphogen gradients
- Bicoid inhibits caudal = which creates tails
- nanos inhibits hunchback

CAM

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14
Q

Necrosis

A

unplanned cell death

  • rupture of cell and spilling contents to surrounding tissue
  • caused by variety of attacks on cell
  • toxins, burns, infection, inflammation
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15
Q

Apoptosis

A

programmed cell death

  • cell chopped up and packaged for removal. DNA fractionated, cell membranes pinch off into small structures
  • fragments labelled for macrophages so they cleaned up through phagocytosis
  1. EGL1 is produced by apoptosis signal
  2. EGL1 binds to CED-9, releasing CED-4
  3. CED-4, released from mitochondria; forms octamers in cytoplasm
  4. CED-4 octamers convert an inactive CED-3 precursor to active CED-3
  5. CED-3 is caspase, destroying various proteins
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16
Q

CED-3

A

when active:
- cleaves lamins (nuclear envelope dissolves)
- activates endonucleases (DNA is digested)
- attacks cytoskeletal components (cell structure)
- attacks cell-cell adhesion proteins (anchors for membrane)
- cleaved (activates) itself (runaway chain reaction)

17
Q

CED-3 mutant

A

no apoptosis

18
Q

CED-4 mutant

A

no apoptosis

19
Q

CED-9 mutant

A

all cells die

20
Q

ED1 mutant

A

no apoptosis

21
Q

Phosphatidylserine (Ps)

A

marks apoptotic particles for phagocytosis
- PS is moved to outside of membrane of apoptotic cells, marking them for phagocytosis by macrophages

22
Q

cancer cells select for mutations in two types of genes

A

proto-oncogenes
- genes that normally promote cell growth. when mutated or amplified they become oncogenes

tumour-suppressor genes
- normally inhibit cell cycle progression. when theyre mutated, cells divide out of control

23
Q

Retinoblastoma

A
  • rare childhood cancer
  • heritable and sporadic cases
  • caused by mutations in Rb gene

= loss of heterozygosity

24
Q

The G1 restriction point is a target of cancer

A
  • Rb rlly important for G1 of cell cycle
  • 2 major kinases in G1 that promote entry into S-phase = G1 CDK + G1/S CDK
  • these kinases phosphorylate Rb
    (if no mitogens = go into G0)
  • restriction point (R or START): cell committed to another round of cell division and is no longer mitogen sensitive
  • Rb represses E2F-E2F promotes expression of replication genes
  • G1 phosphorylates Rb and Rb falls off E2F
25
Q

Rb

A

poor substrate = needs to be phosphorylated multiple times

a repressor of E2F txn factor

26
Q

Inactivation of APC/Cdh1
(new commitment point?)

A

APC/Cdh1 needs to be inactivated before cells enter S-phase
- G1/S CDK phosphorylated Cdh1
- Emi1 leads another Ub ligase to destroy Cdh1

27
Q

p16

A

binds CDK, preventing cyclin/CDK joining. Expression of p16 is driven by stresses placed on the cell

28
Q

G1cyclin/CDKs

A

phosphorylate (inactivat) Rb

29
Q

E2F

A

A TF that drives expression of S-phase genes

30
Q

p53

A

gatekeeper of cell

  • detects conflicts in cell and can activate several pathways to fix them
  • loss of p53 doesn’t make a cancer cell, it predisposes a cell to cancer. occurs through loss of tumour suppressor function
  • ….
31
Q

transcriptional regulation

A
  • distinct genes can be turned on or off
  • distinct mRNAs translated or repressed and localised to different regions of the cell
32
Q

epigenetic regulation

A

marks on DNA that regulate gene expression and are inherited by daughter cells, but independent of DNA sequence

permanently bind Rb to E2F = cell cycle arrest

33
Q

Rb pathway

A
  1. cell signals that it wants to go unto S-phase and so P16 which is inhibiting G1/S CDK goes away (depends on stress of cell - once cell is no longer stressed it released and this continues)
  2. g1 phase = G1/S cyclin binds to CDK and creates complex
  3. G1/S cyclin CDK phosphorylates Rb (which is inhibiting E2F)
  4. Rb leaves E2F and it is activates to create TFs for DNA replication and go into S phase
34
Q

Terminal differentiation

A

permanent cell cycle exit
- differentiated cells become refractory to proliferate signals
- G1/CDK inhibitors and Rb family members play major roles in cell cycle exit
- terminal differentiation is distinct from senescence
(td = permanent withdrawal from cell cycle)

35
Q

Cancer mutations

A

Gain of function = promote proliferation
Loss of function = growth suppress, avoid checkpoints and genomically unstable
Dominant negative = act like loss, mutant bind to wild type

36
Q

Regulation of gene expression

A

Epigenetic: histone acetylation (opens chromatin) and methylation (closes chromatin)
Transcriptional: proteins that promote or inhibit gene expression

biol2200 end of sem (5 decks)

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