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Stem Cells > Stem cells > Flashcards

Stem cells Flashcards

1
Q

3 properties of stem cells …

A
  • Self renewal
  • Potency (can make a no. diff cell types)
  • Differentiation
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2
Q

3 extracellular signals that make the cell grow, divide survive or die

A
  • Growth factors
  • Death factors
  • Survival factors

These cause a change in gene expression leading to self renewal diff. or death

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3
Q

2 main types of EXTERNAL signals

A

-Soluble ligands for receptors
-Internally generated signals
external signals must be carried across the membrane to the nucleus (takes longer)

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4
Q

What must be altered in order to ‘lock’ on/off gene expression

A

Chromatin

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5
Q

Types of chromatin/gene modifications

A
  • DNA methylation (of argines and lysines)
  • Phosphorylation (serine)
  • Histone acetylation (lysines)
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6
Q

What are the 2 main pathways that DNA methylation blocks transcription

A
  • DIRECT BLOCKING OF TFIID binding (TATA binding protein)

- Recruitment of histone deacteylases

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7
Q

Method of transcription

A
  1. )chromatin extends out - EXPOSES ENHANCERS
  2. ) Mediator complex Binds-bridges gap between enhancers
  3. ) Promoter recruits transcription factors
  4. )RNA polymerase transcribes the gene
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8
Q

Splicing

A

introns removed from pre mRNA to produce mRNA

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9
Q

What causes degradation of mRNA ?

A

siRNA

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10
Q

What causes blockage of transcription?

A

miRNA

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11
Q

What destroys proteins

A

Proteasomes degrade ubiquitin tagged proteins

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12
Q

Stages of the cell cycle ?

A
  • G1
  • S
  • G2
  • M
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13
Q

Which stage of the cell cycle has the restriction point (R)?

A

G1

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14
Q

What other phase can cells enter at restriction point

A
  • Cell can enter G0 phase ‘quiescent state’ , stay here until needed
  • CDKs and cyclins disappear
  • can be temporary of lifelong
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15
Q

What occurs at the restriction point in the G1 phase of the cell cycle ?

A
  • somatic cells only
  • key transition point
  • integration of internal and external cues
  • Cells either Commit to S PHASE or enter G0 phase
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16
Q

What are the two checkpoints in the cell cycle ?

A
  • G1 checkpoint

- G2 checkpoint

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17
Q

What is checked at G1 checkpoint ?

A
  • Is cell big enough
  • Is environment favourable
  • Is Dna damaged
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18
Q

What is checked at G2 checkpoint ?

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

(checkpoint must be passed before entering M phase)

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19
Q

What are the three principle components of the cell cycle ?

A 
- Cyclin dependant kinases (CDK)
      Amount stays the same throughout 
-Cyclins 
    Amount fluctuates throughout the cell cycle 
-CDK inhibitor proteins (INK4, KIP)
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20
Q

Cyclin D …

A

Binds with CDK4/6
(G1)
- direct link between extracellular environment and cell cycle
- Growth factors act via up regulation of cyclin D

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21
Q

Cyclin E …

A

Binds with CDK2

G1/S

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22
Q

Cyclin A…

A

Binds with CDK2/1

S+G2

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23
Q

Cyclin B

A

Binds with CDK1

G2/M

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24
Q

Do ES cells have a restriction point ?

A

NO!

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25
Q

Process of restriction point progression

A
  • PRB gets phosphorylated by Cyclin D+ CDK4
  • Cyclin E and CDK2 hyperphosphorylate PRB
  • E2F dissociates +binds to target genes = transcription/ progression
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26
Q

CDK inhibitors

A

INK4 family - prevents cell from entering S phase (binds to CDK4/6)

KIP family - binds to CDK

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27
Q

features of cancer cells

A
  • Cannot arrest at G0
  • loss of G1/S restriction control
  • Unlimited replicative power
  • NO longer responds to growth factors
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28
Q

Importance of cell death

A
  • Digit formation
  • Stopping immune response
  • NS formation
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29
Q

Error in apoptosis can lead to disease…

A

Cancer,HIV,lupus

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30
Q

Too much apoptosis leads to …

A

Tissue atrophy (loss of muscle mass/cells)

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31
Q

Too little apoptosis leads to…

A

Hyperplasia (Increase in organ size)

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32
Q

Characteristics of apoptosis

A
  • PROGRAMMED cell death
  • SHRINKS
  • aggregation of chromatin at nuclear membrane
  • mitochondria release death signals
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33
Q

Characteristics of Necrosis

A
  • UNPROGRAMMED
  • SWELL AND BURST
  • disintegration of organelles
  • NO vesicle formation
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34
Q

Withdrawal of +ve signals and presence of -ve signals leads to …

A

apoptosis

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35
Q

Intrinsic pathway of apoptosis

A

DNA damage+p53 –> mitochondria/cytochrome C
–> INITIATOR CASPASE 9 —> INITIATOR CASPASE 3

…cell death

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36
Q

Extrinsic pathway of apoptosis

A

Death ligands –> Death receptors –>
INITIATOR CASPASE 8 —> INITIATOR CASPASE 3

…cell death

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37
Q

no signals to a cell…

A

leads to cell death

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38
Q

2 main types of signalling methods :

A

-Phosphorylation (kinase and phosphatase)

-GTP-binding protein (GTP binding = activation )
(GTP hydrolysis = inactivation)

The same signal can have many different effects!

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39
Q

3 ways of cell communication

A
  • Direct cell-cell
  • Local (synapses)
  • Hormonal - long range
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40
Q

2 classes of extracellular signalling molecules …

A
  • Small hydrophobic molecules, pass through membrane, activate INTRACELLULAR receptors
  • Hydrophilic Molecules , too large to cross membrane, rely on MEMBRANE RECEPTORS
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41
Q

2 examples of SMALL HYDROPHOBIC molecules

A
  • Steroid hormones

- Nitric Oxide

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42
Q

3 cell surface receptors

A
  • Ion channels
  • G protein coupled receptors
  • Enzyme linked receptors
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43
Q

categories of enzyme linked receptors

A
  • Receptor tyrosine kinases (RTKs), activate AKT pathway = acts as a survival signal that stimulates cell growth/prevents apoptosis
  • Cytokine receptors , growth+diff , direct pathway

-TGF B receptors ,anti proliferative signals
mutations=cancer

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44
Q

Does TGF beta and BMP signalling compete ?

A

YES

  • SMAD 2/3 (Phos. by TGF) competes for SMAD4 (co smad)
  • SMAD 1/5/8(Phos. by BMP) competes for SMAD4 (co smad)
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45
Q

WNT in its OFF state=

A

ubiquitination , no signal

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46
Q

WNT in its ON state=

A

binds to frizzled, activated dishevelled (DVL)

-B-catenin free to turn on target genes (displaces co-repressors)

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47
Q

KINASE INHIBITOR in WNT signalling leads to ….

A

ACTIVATION of pathway

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48
Q

Example of DIRECT cell communication

A

Notch signalling

  • cleaved by gamma secretase (after delta has bound)
  • cleaved domain activates gene transcription
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49
Q

Signalling = patterning of germ layer, what re the 4 main signalling centres ?

A
  1. ) Post. Epiblast (bottom)
  2. ) Anterior Visceral endoderm/AVE (left side)
  3. )Extra Embryonic endoderm (top)
  4. ) The Node (very bottom)
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50
Q

chick model …..Lefty 1 is

A

restricted to DVE

also restricts nodal (which activates it)

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51
Q

chick model …..BMP4 gradient

A

(Induced in nodal epiblast)

-Conc decreases as you go down to node (bottom)

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52
Q

As the embryo grows…

A

AVE+DVE are pushed anteriorly

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53
Q

Primitive streak is SET UP due to ?

A

WNT and TGFB signals which are/have to be restricted to posterior epiblast
-WNT induces TGFB

no signals=ectoderm instead of PS

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54
Q

The NOTOCHORD starts to form at the ?

A

NODE (highest point of NODAL expression)

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55
Q

chick model - Formation of Head/neural structures

A

due to :
-shh +BMP gradients
High BMP= non-neuronal ectoderm
Low BMP= neural crest cells

56
Q

Gastrulation produces 3 Germ layers :

A
  • Ectoderm (skin)
  • Endoderm (gut, liver)
  • Mesoderm (muscle, blood)
57
Q

Primitive streak =

A
  • thicker region on one side

- Epiblast cells migrate through + produce mesoderm and endoderm

58
Q

chick model- Somitogensis/axon formation is caused by ..

A 
FGF + RA levels (give POSTERIOR identity)
Anti WNT (maintain ANTERIOR identities)
59
Q

HIGH POSTERIOR FGF in somitogenisis results in …

A

cell proliferation/axon elongation

60
Q

In chick model - Hensons node forms…

A

Neural tube, somites , notochord

61
Q

In chick model - Primitive streak forms

A

Mesoderm + endoderm

62
Q

In an ES cell for primitive streak use…

A

WNT, Activin TGFB

63
Q

In an ES cell for Ectoderm …

A

BLOCK TGFB and BMP signals

64
Q

In ES cells for Ectoderm patterning…

A

FGF with no BMP +drives neural differentiation

65
Q

what types of cells cannot be gained from human embryos

A

XEN+TS

66
Q

Which stem cells are derived from POST-implantations

A

Epiblast stem cells

67
Q

Where are ES stem cells derived from ?

A

Inner cell mass of blastocysts

68
Q

Properties of ES stem cells

A
  • Non transformed survive forever
  • pluripotent (make all 3 germ layers)
  • stable diploid karyotype
  • HUMAN embryonic stem cells have LOW clonegic capacity
  • carry surface markers
69
Q

Is incorporation of human ES cells into chimera plausible ?

A

NO, and neither is mouse ES cells into humans

70
Q

Are Mouse ES cells Naive ?

A

yes

-dont express lineage markers

71
Q

Mouse EpiSC

A
  • Primed

- express lineage markers

72
Q

Human PSC

A

primed

73
Q

How are human ES cells derived

A

grown in IVF, trophectoderm removed via antibodies

=Leaves inner mass cells

74
Q

4 ways of characterising PSC’s

A
  • Surface markers
  • Genetic
  • epigenetic
  • Gene expression
75
Q

Functional tests for PSC’s

A
  • clonegenic assays
  • 2d,3d differentiation
  • teratoma
76
Q

What can be used for analysis of surface markers

A

flow cytometry

77
Q

mouse ES cell surface marker differences to human ES cells

A
  • all negative APART FROM ALP

- SSEA1 + (positive)

78
Q

marker differentiation caused by

A

inhibiting TGFB and BMP

79
Q

Epigenetic characterisation of PSC’S

A
  • Methylation checking of genes (methylated=on)
    (unmethylated-off)
    -X inactivation Male XY=no inactivation
    Female XX = 1 inactivated
    -Imprinting
80
Q

In epigenetic imprinting genes are exppressed …

A

biallelically
OR
maternally or paternally

81
Q

Physical test of ES cells

A

should be able to form

  • embryos body (plating)
  • organoid
  • monolayer
82
Q

Test for pluripotency

A

teratoma:
inject under skin
ALL 3 GERM LAYERS should form

83
Q

what type of potency are adult stem cells ?
pluripotent
multipotent
unipotent

A

multipotent (some are unipotent)

84
Q

are adult stem cells difficult to maintain in vitro and isolate ?

A

yes, they are very difficult to isolate and maintain in vitro

85
Q

Do adult stem cells have telomerase ?

  • yes
  • no
A

NO, this means they cannot divide indefintely

86
Q

DO adult stem cells fit the Hardwired hierarchy model?

(that adult stem cells have a set limited fate)

A

NO

87
Q

3 reasons why Adult stem cells don’t fit the hardwired hierarchy model

A
  • Not all are multi potent (epidermal basal cells=only kartocytes)
  • Not all are quiescent (intestinal crypt constantly dividing)
  • Not all have a unidirectional cell fate (clara cells in trachea= dedifferentiate into basal stem cell thats damaged)
88
Q

whats the fastest self renewing tissue in a mammal ?

A

Small intestinal- crypt villus unit

= crypt base columnar cells are long term stem cells

89
Q

are there any GO professional stem cells in the intestinal crypt ?

A

NO

90
Q

mammary gland- MaSC are multi potent and give rise to?

A

Myo-sc (unipotent)

lum-sc (bipotent) interconvergance occurs

91
Q

are Satellite cells (muscle stem cells) professional GO stem cells ?

A

YES, but are unipotent (reforms itself and myofibrils to replace damage)

92
Q

What is a STEM CELL NICHE

A

A local tissue that hosts and influences the behaviour and characteristics of stem cells

  • regulates cell diff
  • regulates self renewal
  • HAS DEFINED ANATOMICAL LOCATION
93
Q

What does REMOVAL of stem cells FROM a niche results in ?

A

cellular differentiation (or death)

94
Q

example of niche … In c.elegans as cells move further away what happens

A

they lose niche signal + differentiate

95
Q

Niche concepts :

  • occupancy
  • fate
  • assymetric division
A

occupancy -cell cell adhesions between stem cell and niche keep it near self renewing signals

fate- signals from the niche regulate, self renewal, survival and maintenance

asymmetric divisions- niche can polarise/infulence half of a cell causing asymmetric division

96
Q

Niches provide:

  • physical support
  • soluble factors
  • cell-mediated interactions
A

To MAINTAIN and REGULATE stem cell functions

97
Q

Cells in niches interact with each other through:

A

(i) cell-surface receptors
(ii) Gap junctions
(iii) Soluble factors

98
Q

Examples of niche soluble factors are autocrine and paracrine factors which act locally and diffuse … these factors include ?

A

FGF
WNT
BMPs

99
Q

ECM/Cell adhesion molecules in niches have..

A
  • Spatial cues

- Mechanical inputs

100
Q

What do epigenetic restrictions do ?

A

Prevent a cell from changing from one differentiated state to another

101
Q

What does IPS cells stand for and which cells are induced to produce them ?

A

IPS= Induced pluripotent stem cells , adult cells are induced to become pluripotent , lots of signals and TF’s have to be replicated in order to induce pluripotency

102
Q

What are 2 potential uses of IPS cells

A
  • Disease remodelling

- drug discovery

103
Q

What 3 things have to be reset in order in order to reset the cell state (to produce IPS cells)?

A
  1. ) gene expression (somatic off, embryonic on)
  2. ) methylation (reset to totipotent)
  3. ) chromatin (remodelled)

first example-fibroblasts to muscle- CDNA for myod1

104
Q

example of some signals required to induce pluripotentcy in human cells

A
  • Lentivirus + Oct4, Sox2, Nanog and Lin28

- Retrovirus + Oct4, Sox2, Klf4 and C-Myc

105
Q

some signals required to induce pluripotentcy in human cells also have additional factors , NAME 2

A

Additional factors used to help things – eg SV40Tm hTERT +c-myc these help the cells survive and grow

106
Q

BUT: you are overexpressing factors to drive iPS formation How do you turn the expression off?

A
  • Lentivirus will integrate BUT then be SILENCED.

- Alternative: use a non-integrating method

107
Q

3 examples of non integrating methods of preventing over expression of factors to induce IPS cells

A
  • vector based approaches
  • Protein based approaches (TAT fusion)
  • Chemical based reprogramming
108
Q

Delivery of reprogramming factors to make IPS cells

-VIRUS

A
  • efficient
  • Can integrate instead of being silenced
  • retrovirus, only transduces dividing cells
  • lentivirus , can transduce dividing and non dividing cells
109
Q

Delivery of reprogramming factors to make IPS cells

-Adenovirus + mRNA

A
  • Doesnt integrate

- Very inefficient

110
Q

Delivery of reprogramming factors to make IPS cells

-Transposons

A
  • Efficient

- clones needed for checking of excision ad arrangement

111
Q

Delivery of reprogramming factors to make IPS cells

-Episomal

A
  • Does not use virus

- very inefficient

112
Q

Characteristics of IPS cells…

A
  • Appears any cells can be induced to become IPS cells

- IPS cells carry genotype of parent cells (ES don’t)

113
Q

Why characteristics of IPS cells make them good for disease modelling ?

A

-carry genotype , therefore we can capture a genotype forever

114
Q

HOW are IPS cells used for disease modelling

A

patients somatic cells Compared against normal somatic cells , can then be assessed
-is differentiation different ?
-Is phenotype affected ?
drug screens can be used , and drugs tested on normal cells to see if there is -ve impacts (drug testing)

115
Q

Two forms of AMD

A
  • WET amd (can be treated) -angiogensis +bleeding
  • 90% DRY amd (can’t be treated) - fatty deposits “drusen” between bruch’s membrane and RPE

LOSS OF RETINAL PIGMENT EPITHELIUM in rear of retina
RPE function = regeneration of bleached opsins

costs 8.8 billion per year

116
Q

Treatment procedure of AMD

A

1.)neural retina folded back to reveal RPE layer
2.) RPE cells removed and transplanted
CENTRAL VISION RESTORED AT EXPENSE OF PERIPHERAL VISION

117
Q

produced human Retinal pigment epithelium which restored sight in rats, how was this tested ?

A

-Striped and head tracking to test visual acuity

118
Q

3 issues with cultured adult RPE cells (from post mortem )

A
  • limited donor material
  • hard to grow in vitro
  • degenerate with time with in culture
119
Q

solution of failed attacthent of RPE cells to membrane

A
  • Artificial membrane
  • Artificial choriod
  • Patch (coated with RPE cells)
120
Q

In which disease do Lewy boys get deposited in the brain ?

A

Parkinsons

121
Q

Treatments of parkinson’s ?

A
  • L-dopa (levodopa) can cross BB barrier,dopamine can’t
  • Dopamine agonists
  • MAO inhibitors
  • COMT inhibitors
122
Q

Thalamotry, Pallindotomy and Deep brain stimulation are surgical procedures to treat which disease ?

A

Parkinsons

123
Q

To make dopaminergic neurons from stem cells you have to …

A

inhibit BMP and TGFB signalling

suppress mesodermal diff.

124
Q

specifying dopaminergic neurons

A

-pax6 (anterior fates)
-no morphogens or fgf+wnt inhibition= forebrain
-WNT FGF RA = Caudalize the brain
-midbrain produces - WNT1 FGF8
WNT signalling =patterning of brain

125
Q

gradients of what define the fate of a neuroectodermal precursor on the D/V axis?

A
  • Shh (high at bottom), BMP and WNT (High at top)

- More Shh = more ventral fate

126
Q

Hyperplasia…

A

Increase in no. of cells

reversible

127
Q

Metaplasia…

A

change in cell differentiation (mature)

reversible

128
Q

Dysplasia …

A

change in cell differentiation (less mature)

reversible

129
Q

Neoplasia (cancer) …

A

new abnormal growth of tissue , IRRIVERSIBLE - autonomous

130
Q

Usual fund size in life sciences?

A

£50 million -£300 million

131
Q

proportion of fund used for overheads ?

A

1-2%

132
Q

how is profit split ?

A

80% investors

20% venture fund managers

133
Q

investment + return period ?

A

5-7 years investment

7-10 year return

134
Q

target return from initial investment ?

A

3x

135
Q

Is a patent the right to use/perform the invention ?

A

NO, a patent is NOT the right to perform/use the invention

A patent doesn’t mean you have a monopoly of the market !

136
Q

Which two people murdered people and sold them to doctors for medical research ?

A

William hare

william burke

Stem Cells (1 decks)

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