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SMP > Cell cycle > Flashcards

Cell cycle Flashcards

1
Q

normal cell replication depends on…

A
  1. Mitogens (growth factors)
  2. anchors (must be anchored to ECM)
  3. Contact w/ other cells (contact-inhibited, won’t divide if too crowded)
  4. # of previous divisions (cells = mortal!)
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2
Q

2 basic functions of cell cycle

A
  1. make 2 copies of all genetic info (DNA duplication)

2. get entire genome to each daughter cell (chromosomal segregation)

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3
Q

S phase of cell cycle

A

replication of DNA/chromosomes

Long time (almost half of whole cell cycle), 
*part of interphase
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4
Q

M phase of cell cycle

A 
mitosis (nucleus divides) 
and cytokinesis (cell contents separate)
  • lasts ~ 1 hour out of 24 hr cycle!
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5
Q

“Restriction Point”

A

the checkpoint at end of G1 phase.
where cell determines whether has enough GF and size to replicate
(if not, stays in phase –> “Go”)

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6
Q

Major cell cycle checkpoints

(4)

A
  1. restriction point (end of G1): to divide or not to divide?
  2. S phase checkpoint: is DNA is damaged, and not fixable?
  3. G2/M checkpoint: is replication completed?
  4. Spindle assembly checkpoint (M): are chromatids properly arranged on spindles?
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7
Q

Cyclins (types)

A

Cdk-activating proteins, no separate activity.
4 types:
(needed to pass through checkpoints in each phase of cell cycle)
A = S-cyclins, B = M-cyclins, D = G1-cyclins, E = G1S cyclins

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8
Q

regulation of Cdk activity

A
  1. degrade the cyclin (or the Cdk in some cases)
  2. (de)phosphorylate
  3. Cdk-interfering proteins (CKIs, CIPs, INKs)
  4. transcriptional regulation (of cyclins, CKI, etc.)
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9
Q

Activation of M-Cdk

A
  1. Mitotic cyclin and CDK bind/complex
  2. Wee-1 – adds P to complex
  3. CAK – adds 2nd P to complex
  4. Cdc25 activates the complex (removes 1 P, opens substrate binding site)
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10
Q

CKI

A

Inhibitory molec for Cdks, binds to Cdk-cyclin complex;
wraps around so cannot f(x),
(regardless of what other molecs = present)

  • counteracted by SCF proteosome
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11
Q

cyclin D-Cdk

A

needed by ALL cells, EXCEPT for Embryonic Stem Cells (“ES”),
to pass restriction point.

–> concern: stem cells = naturally tumorigenic (!)

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12
Q

needed for cell cycle “clock”

initiation and progression

A

outside signals:

  • Tyrosine Kinase Rs
  • GPCRs
  • TGF-B Rs
  • NRs AND: nutrient status (will not divide if cell = starving)
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13
Q

G1 checkpoint decision (“regulation point”)

A
  • -> divide (onto S phase) or not divide (to Go phase)
    1. external mitogenic signals –> “we need more cells”
    2. DNA damage??
    3. cell has grown enough?
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14
Q

Mitogens that stimulate D-Cyclins (–> cell proliferation)

A
  1. Growth factor (via Ras or HERneu…)
  2. Wnt pathway
  3. cytkines
  4. NRs
  5. Hedgehog
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15
Q

SCF ubiquitin ligase

A

cell cycle reg. enzyme –> marks CKI for degradation

    • SCF indirectly promotes cell cycle progression **
      1. phosphorylates CKI
      2. CKI = poly-ubiquitinated (by ubiquitin)
  • -> CKI = degraded
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16
Q

TGF-Beta as tumor suppressor

pathways to inhibiting cell prolif.

A

3 ways to inhibit cell proliferation: (at restriction point)

  1. increase expression of CKIs
  2. Block phosphorylation of Rb
  3. Prevent Myc expression
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17
Q

Rb protein

A

regulates cell cycle (inhibits progression) by inhibiting EF2
(EF2 = gene enhancer —> + cell prolif.)
* need >1 phosphorylations of Rb to release from EF2
(phosphorylated by Myc)

18
Q

Contribution of Myc to cell cycle regulation

A
  1. increases phosphorylation of Rb (–> frees EF2)

2. promotes expression of EF2

19
Q

what’s different in Embryonic stem cells for G1 checkpoint?

A
  1. Rb = hyperphosphorylated (–> INactive)
  2. no need for Mitogens
  3. no DNA damage check
  4. Cyclin E = constantly present (NOT degraded)
    - –> can blow through checkpoint w/o actual check!
20
Q

check against mitogen over-stimulation

A
  1. feedback from mitogen stimulation –> Arf (chaperone protein)
  2. Arf sequesters MDM2

*Arf = “14-3-3” (also = Raf inhibitor!)

21
Q

Types of functional mutations in genes to cause cancer

A
  1. bypass need for mitogens
    (act: RTKs, Ras, Cyclin D, PI-3K; INact: PTEN, p53, TFG-Beta)
  2. targeting G1 checkpoints
    (inhibit Rb, p53, CKIs; increase Myc/AP-1)
  3. suppress apoptosis (act: PI-3K; INact: PTEN, p53)
22
Q

Dominant vs. Recessive mutations

A

Dominant: only need mutation in 1 allele

Recessive: must have same mutation in both alleles to exhibit mutation in f(x)

23
Q

Main ways to convert proto-oncogene to oncogene

A
  1. Deletion in DNA – coding gene OR regulatory sequence
  2. mut. transcr. machinery –> change gene expression
  3. Chromosomal rearrangement
    - new reg. sequence
    - fusion to active transcr. gene –> hyperexpression!
24
Q

Most common causes of conversion of proto-oncogene to oncogene

A
  1. Val –> glut (missense mut): no need for mitogens!
  2. single deletion alters transmembrane domain of protein
    - -> R dimerizes w/o ligand!
25
Q

Philadelphia chromosome

A

translocation of tips of chromosomes 9 and 22
–> BCR-ABL fusion protein
(constitutively active tyrosine kinase)

** causes CML (chronic myelogenous leukemia) if in bone marrow

26
Q

Imatinib/gleevac

A

a drug used to treat CML (chronic myelogenous leukemia),

    • specifically targets cancer cells
  • -> no side effects!
27
Q

ways to have normal allele eliminated in heterozygote,

resulting in oncogene expression

A
    • usually = LOH **
      1. non-disjunction 4. chromosome loss and duplication
      2. Mitotic recombination 5. gene conversion
      3. deletion 6. point mutation
28
Q

genetic characteristics of oncogenes

A

Dominant mutations,
gain of function,
* in somatic cells – NOT inherited (fatal in utero)
less tissue preference.

29
Q

genetic characteristics of tumor suppressor genes

A

Recessive mutations (BOTH alleles must be affected),
loss of function,
in germ cell OR somatic cells —> CAN be inherited
*strong tissue preference

30
Q

why not more cancer w/ all cell divisions over lifetime?

A
  1. need 2+ genetic events for cancer (1 mut. is not enough)

2. usually* arise from 1 cell w/ multiple mutations (clonal in origin)

31
Q

Multi-Hit model of cancer induction

A

ALL cells in a tumor should have at least some COMMON genetic alterations.
– evidence: 1. cells from female tumors all have same X-chrom. inactivated; 2. cancer increases w/ age; 3. hard to induce cancer in animals w/ single oncogene; 3. successive muts in pathways

32
Q

Rb regulates which checkpoint type?

A

Rb:

regulates “Regulatory Point” (checkpoint)

33
Q

p53 regulates which checkpoint type?

A

p53:
regulates DNA Damage checkpoints

(aka: “guardian of the genome”)

34
Q

dominant negative mutation

A

a genetic mutation in a single allele which inhibits the function of the other (wild type) allele

  • -> acts as dominant mutation.
    ie: Li-Fraumeni syndrome (affects p53 function)
35
Q

meiosis

A

1 round of DNA synthesis (replication),
2 successive rounds of cell division
(w/ chromosomal segregation)

36
Q

major gametogenesis trigger

A

RA (retinoic acid),
binds to nuclear receptors.
responsible for regulating the timing of cells entering mitosis

37
Q

Splitting cell organelles in mitosis

A
  • Key: want to split evenly, helped by cytoskeleton.
  • Mitochondria: double number, (so ubiquitous that this is enough)
  • All others (Golgi, ER): fragment into small pieces then regrow
    (Increases chance to split evenly btwn new cells)
38
Q

Cdk (cyclin dependent kinases)

A

Category of enzymes, for cell cycle regulation.
Activated by binding cyclins,

Active: phosphorylates cell cycle proteins

39
Q

G1 cyclins

A

w/ Cdk –> regulate activity of G1S cyclins;
- activated by mitogens

D cyclin

40
Q

G1S cyclins

A

In late G1, bind to Cdks to help pass restriction point;
(Promote commitment into cell cycle)

E cyclin

41
Q

S cyclins

A

Right after restriction point,
Bind to Cdks to stimulate chromosome duplication.
(Control early Mitotic events)
A cyclins

42
Q

M cyclins

A

Bind to Cdks,
–> stimulate entry into mitosis (M phase)

B cyclins

SMP (8 decks)

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