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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
Q

What about G0?

A

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
Q

what are these describing:

  • fundamental alterations in the genetic control of cell division
  • normal cell cycle regulatory mechanisms are lost
A

CANCER

27
Q

typical features of cancer cells:

A
  • 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
Q

what the key cell cycle transition point

A

G1/S

29
Q

whats the cell cycle regulated by:

A

cyclin-CDK complexes

30
Q

cells are balanced between

A

life & death

31
Q

normal cell with survival cues & proliferation cues =

A

SURVIVAL & PROLIFERATION

32
Q

normal cell surviving & proliferating given death signal results in

A

death cues + growth inhibition cues –> CELL DEATH, NO DIVISION

33
Q

normal cell received death signal converted to CANCER signal =

A

SURVIVAL CUES + PROLIFERATION CUES (LOTS) = Uncontrolled survival & proliferation

34
Q

apoptosis =

A

programmed cell death

35
Q

apoptosis examples:

A
  • 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
Q

malfunction of apoptosis leads to diseases such as:

A
  • Cancer (TNF produced by macrophages activates extrinsic pathway)
  • Neurodegenerative diseases
  • AIDS (HIV deactivates Bcl-2)
  • Ischemic stroke
  • Autoimmune disease (lupus)
37
Q

apoptosis: role in disease (too much/too little)

A

right amount = homeostasis
TOO MUCH = tissue atrophy –> Neurodegeneration, thin skin etc.
TOO LITTE = hyperplasia –> Cancer. atherosclerosis etc

38
Q

apoptosis: role in a Stem cell’s biology

A

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
Q

necrosis

A

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
Q

apoptosis: (Steps)

A
  • no loss of integrity
  • aggregation of chromatin at nuclear membrane
  • shrinking of cytoplasm and nuclear condensation
  • mitochondria release death signals
41
Q

Necrosis (steps):

A 
• Loss of membrane integrity
• Swelling of the cytoplasm and
mitochondria
• Total cell lysis
• Disintegration of organelles 
• No vesicle formation
42
Q

when is apoptosis important?

A
  • 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
Q

when is apoptosis important? development & morphogenesis

A 
• Eliminatesexcesscells:
- tadpole tail metamorphosis - nervous system
- immune system
• Eliminatesnon-functionalcells:
- interdigital mesenchymal tissue
- formation of reproductive organs
44
Q

when is apoptosis important? Adults

A
  • 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
Q

when is apoptosis important? Cells infected with viruses

A

Cytotoxic T-lymphocytes (CTLs) kill virus-infected cells

46
Q

when is apoptosis important? cells of the immune system

A

After prolonged cell-mediated immune responses => body removes effector cells

47
Q

when is apoptosis important? Cells with DNA damage

A

Damage to the genome causes a cell to become cancerous

48
Q

when is apoptosis important?Cancer cells

A

Cancer therapy induces apoptosis

49
Q

what makes a cell decide to commit suicide?

A
  • 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
Q

stages of apoptosis (4)

A
  • Healthy cells get the death signal
  • commitment to die (reversible) turns into execution (irreversible)
  • Dead cell (condensed) is engulfed
  • leads to degradation
51
Q

Assays to detect apoptotic cells: DNA fragmentation

A

“DNA ladder” on electrophoresis

52
Q

Assays to detect apoptotic cells: Morphological changes

A

Nuclear blabbing & fragmentation cell shrinkage

53
Q

Assays to detect apoptotic cells:Loss of plasma membrane integrity

A

Loss of dye exclusion (e.g. trepan blue, acridine organs)

54
Q

caspases cleave proteins involved in

A
  • inhibiting apoptosis
  • DNA repair
  • cell cycle
  • nuclear structure
55
Q

intrinsic =

A

belonging naturally; essential

56
Q

extrinsic =

A

not part of the essential nature of someone or somethin

57
Q

Intrinsic apoptosis pathways:

A
  • DNA damage & p53
  • Mitochondria/ cytochrome C
  • Initiator caspase 9
  • Effector caspase 3
  • APOPTOSIS
58
Q

Extrinsic apoptosis pathways:

A
  • Death Ligands
  • Death receptors
  • initiator caspase 8
  • effector caspase 3
  • APOPTOSIS
59
Q

what causes differentiation

A

Changes in Gene expression

-Changes in protein expression/function

BMS 114: Stem cells (16 decks)

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