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Cell Bio > Cell Cycle and Apoptosis > Flashcards

Cell Cycle and Apoptosis Flashcards

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Biology 101 flashcards
1
Q

4 major phases of the cell cycle

A

G1, S, G2: Interphase

M

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2
Q

G0 phase

A

Cell is no longer dividing
Quiescent (dormant)
Can re-enter cell cycle

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3
Q

M phase

A

Cell division

2 parts: mitosis (nuclear division) and cytokinesis (cytoplasmic division)

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4
Q

Prophase/Prometaphase

A

Chromosomes condense
Nuclear envelope breaks down
Mitotic spindle (microtubules) forms
Kinetochore (protein structure at centromere) connects chromosomes to microtubules
Centrosomes (organizing centers) form at opposite sides of cells

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5
Q

Metaphase

A

Centromeres line up at metaphase plate

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6
Q

Anaphase

A

Sister chromatids separate

Kinetochores pull chromosomes along microtubules

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7
Q

Telophase

A

Two daughter nuclei form

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8
Q

G1 phase

A

Cell grows and makes more macromolecules and organelles

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9
Q

S phase

A

DNA is replicated

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10
Q

G2 phase

A

Cell grows and makes more materials as in G1

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11
Q

3 major checkpoints in the cell cycle

A

End of G1
End of G2
Partway through M
Cell machinery is always surveying the state of the cell

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12
Q

G1 checkpoint

A

Make sure that there is enough material to replicate DNA

Look for DNA damage

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13
Q

G2 checkpoint

A

Make sure that DNA has been duplicated completely and correctly

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14
Q

M checkpoint

A

Make sure that mitotic spindles are attached properly and that there is enough material to make daughter cells

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15
Q

2 major proteins involved in checkpoints

A

Cyclins

Cyclin-dependent kinases (Cdks)

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16
Q

Cyclin-Cdk complex

A

Cyclin binds to Cdk -> Cdk changes shape -> kinase ability is activated (Cdk can phosphorylate key proteins that initiate the next step in the cell cycle)
More cyclin present- greater Cdk activity

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17
Q

Specificity of cyclin-Cdk

A

Specific cyclin-Cdk complexes exist for each checkpoint

Different targets are phosphorylated to activate next step

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18
Q

Cdc6 and cyclin-Cdk complex

A

G1: Cdc6 (protein) is bound to origin recognition complex (ORC), which is bound to origin of replication
Cdc6 + ORC + origin of replication = pre-replicative complex
S: S-Cdk triggers S phase -> Cdc6 is phosphorylated and then degraded -> replication fork assembled -> DNA replication
Cdc6 phosphorylation: beginning of transcription
Once Cdc6 is phosphorylated, origin of replication can’t be used again

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19
Q

Regulation of cyclin-Cdk complex

A

Cdk is phosphorylated and then dephosphorylated to turn on
Cyclin is degraded to turn off
Cdk inhibitor proteins can hold back or turn off completely
Extracellular cues

20
Q

Phosphorylation of cyclin-Cdk complex

A

Cdk is phosphorylated and de-phosphorylated according to cellular cues
Cyclin binds to Cdk -> protein kinases phosphorylate Cdk -> activating protein phosphatase removes inhibitory phosphate, leaving activating phosphate -> active cyclin-Cdk complex

21
Q

Ubiquitylation of cyclin-Cdk complex

A

Allows for Cdk to be deactivated
Ub-ligase attaches ubiquitin to cyclin, tagging it for proteosome
Proteosome degrades cyclin

22
Q

Inhibitor proteins

A

Proteins inhibit formation of cyclin-Cdk or cyclin-Cdk activity
DNA damage activates protein kinases that activate p53 protein -> active p53 binds to regulatory region of p21 gene -> transcription and then translation of p21 gene -> p21 protein binds to cyclin-Cdk complex, inhibiting it

23
Q

Survival factors

A

Inhibit apoptosis

24
Q

Mitogens

A

Stimulate cell division by activating corresponding cell cycle cascade
Mitogen binds to mitogen receptor in cell membrane -> mitogen-activated protein (MAP) kinase cascade -> activation of Cdk -> Rb protein is phosphorylated -> Rb lets go of transcription factor -> cell proliferation

25
Q

Growth factors

A

Stimulate cell growth

Activate signaling cascade -> increased production of macromolecules

26
Q

Components of cytoskeleton that aid in cell division

A

Mitotic spindle

Contractile ring

27
Q

Contractile ring

A

Actin and myosin assemble on cytoplasmic face of plasma membrane
Slide like muscle contraction, pulling membrane in

28
Q

Phragmoblasts

A

Found in plants
Construct cell wall as final step in cell division
Phragmoblast microtubules position Golgi-derived membrane to form new cell wall

29
Q

3 classes of microtubules

A

Kinetochore microtubules
Aster microtubules
Interpolar microtubules
All 3 types array from centrosome

30
Q

Kinetochore microtubules

A

Attach to centromere and pull chromosomes apart as they (MTs) shorten

31
Q

Aster microtubules

A

Pull centrosomes apart

32
Q

Interpolar microtubules

A

Push poles apart using sliding force

33
Q

Timing of assembly of mitotic spindle

A

Centrosomes replicate during interphase and migrate during M phase

34
Q

Dead cells

A

Loss of integrity of plasma membrane
Cell, including nucleus, has undergone complete fragmentation into discrete apoptotic bodies and/or its corpse or fragments has been engulfed by an adjacent cell

35
Q

Causes of cell death

A

Damage to cell (DNA, ER, oxidative stress, etc.)
Cell is no longer working efficiently
Development (“webbing” between fingers disappears in embryo)

36
Q

2 types of cell death

A

Necrosis

Apoptosis

37
Q

Necrosis

A

“Messy” death
Acute injury causes cell to lyse and dump its components
Compromising of cell membrane

38
Q

Apoptosis

A 
"Neat" death
Cell is engulfed by phagocytic cell and cellular components are recycled
Compartmentalized
No damage to neighboring cells
Complex signaling cascade
39
Q

Vacuoles in apoptosis

A

Vacuoles become enlarged: cell partitions itself off

40
Q

What happens to cell during apoptosis

A
  1. Blebbing of cell: cytoskeleton uncouples from membrane and ball-like structures (blebs-contain cell components) form
  2. Cell shrinks
  3. Nucleus fragments
  4. Chromatin condenses
  5. DNA fragments
41
Q

2 major pro-aptotic pathways

A

Extrinsic: extracellular cues induce
Intrinsic: cellular damage induces (causes activation through mitochondria)

42
Q

Intrinsic apoptotic pathway

A
  1. Cell stress activates BAX
  2. BAX causes permeabilization of mitochondria
  3. Cytochrome C leaks out (cytochrome C: electron transport chain- end of energy production, committed step)
  4. Apoptosome forms
  5. Apoptotic processes activated by caspases
43
Q

Extrinsic apoptotic pathway

A
  1. 1st messenger binds to death receptor
  2. Caspases activate BAX
  3. BAX causes permeabilization of mitochondria
  4. Cytochrome C leaks out
  5. Apoptosome forms
  6. Apoptosis by caspases
    OR
    Caspases that activate BAX also activate caspases that cause apoptosis
44
Q

Bcl2 protein

A

Anti-aptotic: inhibits BAX

45
Q

Caspases

A

Proteases (cleave proteins)
Activated by cleavage
To activate: cleave procaspase
Regulate apoptosis using irreversible method (cleavage is permanent): cell is damaged- don’t want to go back
1 molecule of this can cleave many molecules of this, which in turn cleave more molecules of this

46
Q

Ways to measure apoptosis

A

Cleaved caspase 3 (Western blot: Ab on cleaved caspase)
TUNEL stain: label ends of chopped-up DNA and look at it under microscope
Phosphoserine exposure: phospholipids are flipped to outer side of membrane during apoptosis (usually on inner)

47
Q

Phosphoserine exposure

A

Annexin 5 binds to phosphoserine
Use Ab to Annexin 5 to label apoptotic cells
Measure Ab binding by flow cytometry (control graph: no shoulder; experimental graph: shoulder)

Cell Bio (15 decks)

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