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BMS 114: Stem cells > Lecture 4: Basic Molecular Cell Biology II > Flashcards

Lecture 4: Basic Molecular Cell Biology II Flashcards

1
Q

A stem cell is a (relatively) primitive cell that is a capable of:

A
  • self renewal - making a copy of oneself
  • make a range of cell types (potency)
  • convert to a different cell type (differentiation)
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2
Q

the features of stem cells allow them to :

A
  • build embryos & tissues (development)

- repairs tissues (regeneration)

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3
Q

choices stem cells can make:

A
  • self renewal
  • differentiation
  • death
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4
Q

self renewal: the cell cycle

A

1) Cell growth + chromosome replication
2) chromosome segregation
3) cell division

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5
Q

cell cycle phases:

A

interphase: main part of cell cycle
- G1 phase
- S phase
- G2 phase

MITOSIS: cell division
Sub-phases:- prophase, prometaphase, metaphase, anaphase, telophase
-cytokinesis

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6
Q

what happens in G1 phase

A
  • cell increases in size
  • ribosome, RNA produced
  • preparation for DNA synthesis
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7
Q

what happens in S phase:

A

-DNA synthesised (chromosomes duplicated)

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8
Q

What happens in G2 phase:

A
  • cell check fidelity of DNA

- preparation for nuclear division

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9
Q

Cell cycle checkpoints:

A

-G1
-G2
-metaphase checkpoint
(during G1 option to go into G0 –> nothing occurs in this state)

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10
Q

G1 checkpoint checks for

A

Is cell big enough?

Is environment favourable? DNA damage?

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11
Q

G2 checkpoints checks for

A
  • Is all DNA replicated?
  • is cell big enough?
  • is environment favourable?
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12
Q

Metaphase checkpoint checks for?

A

Are all chromosome aligned ons spindle?

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13
Q

THREE basic cell cycle principle components

A
  1. Cyclin dependent kinases (CDK)
    - serine/threonine kinases
    - constitutively expressed
  2. Cyclins
    - periodic synthesis and degradation
  3. CDK inhibitor proteins
    - non-kinase inhibitors (INK4 and KIP)
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14
Q

mammalian cyclin-CDK complexes

A

increased complexity in mammalian cells: cyclins A-T, CDK 1-9

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15
Q

expression of each cyclin is limited to

A

a specific cell cycles phase

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16
Q

each cyclin binds with a specific CDK partner:

A

Cyclin D –> CDK4/6 (G1)
Cyclin E –> CDK2 (G1/S)
Cyclin A –> CDK2/1 (S+G2)
Cyclin B –> CDK1 (G2/M)

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17
Q

Cyclin D is the direct link between

A

the extracellular environments and the cell cycle

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18
Q

how do most growth factors act by

A

directly up-regulating Cyclin D expression. i.e. promoting SELF-RENEWAL

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19
Q

The G1/S restriction point

A
  • Key transition point in the mammalian cell cycle
  • integration of
  • -internal cues e..g growth rate & cell size
  • -external cues e.g. proliferate/anti-proliferate factors
  • the cell will commit to division and process into S-phase OR exit the cell cycle to G0
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20
Q

Restriction point =

A

point of no return, the cell is committed to complete the reminder of the cell cycle

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21
Q

for cell to pass R point what must happen

A

Cyclin E bind to CDK2 enter S phase

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22
Q

CDK inhibitor proteins

A

INK4 Family

KIP Family

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23
Q

INK4 Family

A 
- Inhibitor of CDK4 - Family members:
p16INK4A,
p15INK4B, p18INK4C,
p19INK4D
- Binary inhibitors
- Prohibit cyclin binding
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24
Q

KIP Family

A
  • CDK Inhibitor Protein
  • Family members: p21CIP1, p27KIP1, p57KIP2
  • Ternary inhibitors
  • Prevent cyclin-CDK activation
25
What about G0?
Cells can withdraw from the cell cycle and dismantle the regulatory machinery - G0 is a quiescent state - Cdks and cyclins disappear - Some cells enter G0 temporarily & divide infrequently (i.e. hepatocytes ) - other differentiated cell types (neutrons) spend their life in G0
26
what are these describing: - fundamental alterations in the genetic control of cell division - normal cell cycle regulatory mechanisms are lost
CANCER
27
typical features of cancer cells:
- cannot arrest at G0 - loss of G1/S restriction point control - failure to respond appropriately to growth factor signals - - positive growth factors, e.g. EGF - - negative growth factors, e.g. TGF-beta - cells do NOT have a limited replicative life span - LOSS of contact inhibition - --> consequence is unrestrained cell proliferation
28
what the key cell cycle transition point
G1/S
29
whats the cell cycle regulated by:
cyclin-CDK complexes
30
cells are balanced between
life & death
31
normal cell with survival cues & proliferation cues =
SURVIVAL & PROLIFERATION
32
normal cell surviving & proliferating given death signal results in
death cues + growth inhibition cues --> CELL DEATH, NO DIVISION
33
normal cell received death signal converted to CANCER signal =
SURVIVAL CUES + PROLIFERATION CUES (LOTS) = Uncontrolled survival & proliferation
34
apoptosis =
programmed cell death
35
apoptosis examples:
* Embryonic morphogenesis * Killing by immune effector cells * Wiring of the developing nervous system * Regulation of cell viability by hormones and growth factors (most cells die if they fail to receive survival signals from other cells)
36
malfunction of apoptosis leads to diseases such as:
* Cancer (TNF produced by macrophages activates extrinsic pathway) * Neurodegenerative diseases * AIDS (HIV deactivates Bcl-2) * Ischemic stroke * Autoimmune disease (lupus)
37
apoptosis: role in disease (too much/too little)
right amount = homeostasis TOO MUCH = tissue atrophy --> Neurodegeneration, thin skin etc. TOO LITTE = hyperplasia --> Cancer. atherosclerosis etc
38
apoptosis: role in a Stem cell's biology
right amount = homeostasis TOO MUCH = loss of stem cells. Problems with regeneration TOO LITTLE = Too many stem cells. Problems with regeneration and function e.g. leukemia
39
necrosis
the death of most or all of the cells in an organ or tissue due to disease, injury, or failure of the blood supply.
40
apoptosis: (Steps)
- no loss of integrity - aggregation of chromatin at nuclear membrane - shrinking of cytoplasm and nuclear condensation - mitochondria release death signals
41
Necrosis (steps):
``` • Loss of membrane integrity • Swelling of the cytoplasm and mitochondria • Total cell lysis • Disintegration of organelles • No vesicle formation ```
42
when is apoptosis important?
- developement and Morphogenesis - Adults - Destorys cells that represent a threat to the integrity of the organism (cells infected with viruses, of the immune system, with DNA damage,cancer cells)
43
when is apoptosis important? development & morphogenesis
``` • Eliminatesexcesscells: - tadpole tail metamorphosis - nervous system - immune system • Eliminatesnon-functionalcells: - interdigital mesenchymal tissue - formation of reproductive organs ```
44
when is apoptosis important? Adults
- Tissue remodelling/ maintenance - The loss of the endometrium at the start of menstruation - Maintains organ size and function by balancing out proliferation (liver, intestine)
45
when is apoptosis important? Cells infected with viruses
Cytotoxic T-lymphocytes (CTLs) kill virus-infected cells
46
when is apoptosis important? cells of the immune system
After prolonged cell-mediated immune responses => body removes effector cells
47
when is apoptosis important? Cells with DNA damage
Damage to the genome causes a cell to become cancerous
48
when is apoptosis important?Cancer cells
Cancer therapy induces apoptosis
49
what makes a cell decide to commit suicide?
- Withdrawal of positive signals - -surviva; of cells requires - --continuous stimulation from other cells - --continues adhesion - Presence of negative signals - -increase levels of free radicals and oxidants - -DNA-related inducers i.e. UV light - -physiological activators i.e. growth factor withdrawal
50
stages of apoptosis (4)
- Healthy cells get the death signal - commitment to die (reversible) turns into execution (irreversible) - Dead cell (condensed) is engulfed - leads to degradation
51
Assays to detect apoptotic cells: DNA fragmentation
"DNA ladder" on electrophoresis
52
Assays to detect apoptotic cells: Morphological changes
Nuclear blabbing & fragmentation cell shrinkage
53
Assays to detect apoptotic cells:Loss of plasma membrane integrity
Loss of dye exclusion (e.g. trepan blue, acridine organs)
54
caspases cleave proteins involved in
- inhibiting apoptosis - DNA repair - cell cycle - nuclear structure
55
intrinsic =
belonging naturally; essential
56
extrinsic =
not part of the essential nature of someone or somethin
57
Intrinsic apoptosis pathways:
- DNA damage & p53 - Mitochondria/ cytochrome C - Initiator caspase 9 - Effector caspase 3 - APOPTOSIS
58
Extrinsic apoptosis pathways:
- Death Ligands - Death receptors - initiator caspase 8 - effector caspase 3 - APOPTOSIS
59
what causes differentiation
Changes in Gene expression | -Changes in protein expression/function

BMS 114: Stem cells (16 decks)

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