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Block 1 Week 2 > Cell Cycle > Flashcards

Cell Cycle Flashcards

1
Q

Phases of the cell cycle?

A

1) G1
2) S
3) G2
4) M phase (mitosis+ cytokinesis)
5) G0

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2
Q

During G1 of the cell cycle?

A
  • proteins required for DNA rep. made

- cellular components(except chromosomes) are duplicated

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3
Q

In S phase of the cell cycle?

A

1) chromosomes create multiple origins of rep.
2) DNA synthesis initiated at same time at all origins of rep. along the chromosome
- done bilaterally
- end up with each of 46 chromosomes duplicated

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4
Q

In G2 phase of the cell cycle?

A

cell double checks the duplicated chromosomes for errors

-does repairs if needed before move to mitosis

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5
Q

What is the G0 phase?

A
  • cells that drop out of mitosis; are not proliferating
  • adult differentiated cells, are arrested here if no more mitosis is needed
  • cells here CAN re-enter G1
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6
Q

shortest portion of the cell cycle?

A

-mitosis, but is carefully choreographed to ensure each daughter cell gets a all the chromosomes

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7
Q

Mitosis vs. meiosis? What do we want from mitosis? Whats the exception?

A
  • meisosis is a reduction division, mitosis is not
  • creates two genetically identical daughter cells in
  • identical EXCEPT for mitochondria which can vary
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8
Q

how much do most cells in a healthy human divide?

A
  • most cells aren’t actively dividing; but some like hair/gut do
  • regulation of cell division is defining feature of differentiation program in each cell
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9
Q

regulation of cell division(env. vs terminal differentiation)?

A

1) cells produced by dividing stem cell population that undergo terminal differentiation and loose ability to divide (erythrocytes)
2) cells retain ability to divide but only in response to env cues like damage/repair (hepatocytes)

cells can go back & forth

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10
Q

Flow cytometric detection?

A
  • nonspecific DNA binding used to tag cells & track cell division
  • use fluorescence to take cells to quantify them
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11
Q

Flow cytometric detection of cell proliferation & ploidy?

A

should see:

1) see a lot of cells in G1/G0 since where most arrest(PEAK)
2) S phase cells are less but have a lot more DNA in them
3) more cells in M and G2 (second, lower PEAK)

  • diploid (1x); haploid=.5x
  • tumors will be all over map, no two defined peaks
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12
Q

what are telomeres?

A
  • repetitive bits of sequence added at the tips of chromosomes but TELOMERASE
  • required to maintain chromosomal integrity
  • w/o chromosomes would loose genetic material w/ each cell division
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13
Q

How is DNA replicated in S phase? What does it mean?

A

by semi-conservative DNA synthesis (5’–>3’)
-means that after replication, each new daughter cell double helix has one NEWLY synthesized strand & one old DNA strand

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14
Q

steps of DNA replication, leading vs lagging strand?

A

1) polymerase works 5’–>3’ at every origin of replication bubble on chromosome
2) leading strand 5’–>3’ is moving WITH helices as it unwinds DNA
3) lagging strand 5’->3’ moves OPPOSITE to helices
- ogazaki fragments
4) require DNA repair to link Okazaki fragments
5) polymerase runs out of room, can’t add the last few nucleotides on 3’ end which are telomeres
- is why loose telomeres each cycle

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15
Q

cell cycle and telomeres

A
  • telomerase adds repetitive sequences (telomeres) to tip of chromosomes
  • these sequences are shortened w/ each cell division
  • w/o telomeres would loose coding genetic material w/ each round of cell division
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16
Q

Dyskeratosis congenita?

A
  • premature aging disease caused by a lack of telomeres

- DNA being damaged, triggers adpoptosis & senescence (halted cell division)–> premature aging

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17
Q

chromosomes compaction status during cell cycle?

A

1) cell cycle moves into mitosis, chromosomes contract into VERY condensed state
- when stained w/ giemsa are visible in light microscope

2)after M chromosomes de-condense/uncoil

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18
Q

How cell cycle regulated?

A

-actively regulated by checkpoints (go/no-go)

that ensure each step is complete & env is sufficient for division

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19
Q

go/no-go check points? when disregulated?

A
  • where many errors occur & must be controlled
  • genetic errors in checkpoints can be crucial
  • dysregulation of check points contributes to oncogenesis (Cancer) & failure of tissue repair
  • checkpoints REGULATE activity of cell cycle
20
Q

1) G1 checkpoint?
2) G2 checkpoint
3) Metaphase checkpoint?

A

1) is env. favorable for proliferation?
2) is all DNA replicated? is env. favorable?
3) are all chromosomes attached to the spindle?

21
Q

cell cycle phases length of time?

A 
G1= 10 hours
S= 7.5 hours 
G2= 3.5 hours 
M= 1.0 hours

-in a cell w/ 22 hr generation time

22
Q

cyclin dependent kinases (cdk) and cyclins?

A
  • cyclins= regulatory subunit, CDK= their receptor; work as complex
  • have many diff CDK/cyclins for diff parts of the cell
  • can regulate how/when cyclins bind CDK; when want to stop mitosis we degrade them
  • regulate the cell cycle
23
Q

M-cyclin?

A
  • binds to specific Cdk (now M-CDK); which goes to trigger mitosis in between G2 and M phases
  • signals then sent to degrade M-cyclin & stop mitosis
24
Q

S-cyclin?

A

1) S-cyclin activated in G1
2) cyclin binds CDK (now S-Cdk) between G1 & S
3) S-cyclin degraded in S, CDK released, rep. stops

25
Q

phosphorylation activating or deactivating?

A
  • can be both depending on which molecule it is & the site on the molecule
  • phosph. adds charge which changes conformation of binding pocket & how it binds to other molecules
26
Q

4 types of cyclin?

A 
Cyclin D (G1 phase)
Cyclin E (G1/S phase)
Cyclin A (G2 phase)
Cyclin B (Mitosis)
27
Q

cyclin D?

A
  • triggers cells to move from G0 to G1 and from G1 to S phase
28
Q

Cyclin E

A

-prepares the cell for DNA replication in S phase

29
Q

Cyclin A

A

activates DNA replication inside the nucleus in S phase

30
Q

Cyclin B

A

promotes assembly of mitotic spindle in cytoplasm to prepare for mitosis

31
Q

how are stage-specific cyclins controlled?

A

-by APC and CD34 that degrade cyclins

APC= anaphase promoting complex

32
Q

p27 structure, function, role? What happens when lost?

A
  • is a cyclin, binds specific CDK in G0
  • when BOUND prevents exit from G0
  • p27 mutations associated w/ cancer since lost ability to inhibit
33
Q

How does Cyclin D & E cell cycle regulation?

A
  • together regulate G1 phase by regulating activation of Rb & E2F-1
    1) unphosph. RB forms complex w/ E2F1 (no trxn)
    2) phosphorylation of Rb promotes dissociation from E2F1 (trxn begins)
    3) E2F1 makes cyclin A RNA
34
Q

Cyclin A regulation?

A
  • once rb is phosphorylated & unbinds E2F1, RNA of cyclin A–> cyclin protein &binds CDK2
  • this allows us to move from S–> G2
35
Q

cyclin B regualtion?

A

1) B cyclin is bound to phosphorylated cdc2;
2) once cyclin A is activated; cdc2 is dephosphoryalted
3) allows entrance into M phase

36
Q

hijacking of Rb?

A
  • gets hijacked by cancer & viruses

- Rb remains unphosph., bound to E2F1 & E2F1 can’t make RNA needed to make cyclin A

37
Q

what is phosphorylated rb?

A

-Cyclin D &CDK4/6 do initial phosphorylation
-mid G1
Cyclin E & CDK2 finish job
-late G1
-Rb has multiple phos. sites that must be phosphorylated in correct order

38
Q

HPV (human papilloma virus) & Rb regulation?

A
  • HPV hijacks Rb so can’t bind E2F1; causes E2F1 to be free to trxn cyclin A w/o regulation
  • promotes cell division which is good for virus cuz gets more viral factories
  • bad for humans
39
Q

p53 activation/steps?

A
  • activated by phosph. in response to any direct DNA damage (X-rays, chemicals etc)
  • phosph p53 is more stable (not easily degraded) triggers trxn of p21
    3) p21 locks CDK in off postion, promoting cell cycle arrest
40
Q

p53?

A

Activated p53 promotes cell cycle arrest so is a tumor suppressor
-is not always inactive or else wouldn’t be able to do wound healing or repair tissue damage

41
Q

p53 mutations?

A
  • cause Li Frameini (multiple cancers in diff organs since cell cycle lost inhibition)
  • can cause somatic mutations leading to cancer
42
Q

somatic mutations?

A
  • occur in adult life, can’t be passed to children since not germ cell
  • often occur in cancer & often signal progression to malignant phase
  • if somatic mutation t p53 happen in parent cell, then it’s daughter cells now have it & there daughter cells have it etc etc
  • leads to slow accumulation of p53 deactivated cancer cells
43
Q

CIP proteins?

A
  • cdk inhibitory proteins
  • inhibit all cdk/cyclin complexes
  • p21= mediates p53 directed cell cycle arrest
44
Q

INK4 proteins?

A
  • inhibitors of kinase 4
  • only inhibit cyclin D-cdk4/6 complexes
  • which prevent phosphorylation of Rb & prevents trxn of cyclin A, prevents cell cycle progression (TUMOR SUPRESSOR)
45
Q

what is RB?

A
  • retinoblastoma protein

- trxn regulator that is the gatekeeper for exit from G1–>S

Block 1 Week 2 (9 decks)

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