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My Packs: UWO (BIO 1002) > Cycle 8+9 Workshop > Flashcards

Cycle 8+9 Workshop Flashcards

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Biology 101 flashcards
1
Q

Define:

Stem cells

A

Cells that are able to differentiate into multiple types of cells

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2
Q

List:

Types of stem cells

A
  • Embryonic
  • Somatic
  • iPS
  • Umbilical cord stem cells
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3
Q

How are stem cells different from normal cells?

A

They have to express telomerase as they persist for much longer than normal cells and have to maintain telomere length

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4
Q

Where do umbilical stem stells come from?

A

Come from embryogenesis and some stay with us in adult life

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5
Q

List and define:

Potency/origin of stem cells

A
  1. Totipotent: Can form an entire viable organism
  2. Pluripotent: Can form nearly all cells
  3. Multipotent: Can differentiate into a family of cells
  4. Unipotent: Can only form one cell type
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6
Q

Give an example of:

Totipotent cell

A

Only the zygote is totipotent

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7
Q

Give an example of:

Pluripotent cells

A

Nearly all cells

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8
Q

Give an example of:

Multipotent cells

A

Cells of a specific tissue type

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9
Q

Give an example of:

Unipotent cell

A

Epidermal cells

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10
Q

State the difference between:

Somatic cell and a Unipotent Stem Cell

A

Unipotent stem cells
* Give rise to cells that won’t reach cell senescence (self-renew)

Somatic cells
* Eventually reach their Hayflick limit, must enter irreversible cell cycle arrest

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11
Q

True or False:

All stem cells have the exact same genome

A

True

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12
Q

What are the two types of regulation of gene expression that determine what cell type a stem cell can give rise to?

A

Temporal
Spatial

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13
Q

What plays a big role in determining the type of cell the stem cell give rise to?

A

Tissue-specific transcription factors

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14
Q

Define:

Spatial regulation (in terms of stem cell regulation)

A

Where (in what cell/part of the body)

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15
Q

Define:

Temporal regulation (in terms of stem cell regulation)

A

When (at what time/under what conditions)

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16
Q

List:

The stages that we can control gene expression

A
  • Transcription
  • Post-transcription
  • Translation
  • Post-translation
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17
Q

Why is regulation at the transcriptional level very important?

A

Prevents the waste of resources and energy to transcribe a protein when it is halted down the process line

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18
Q

What is transcription controlled by?

A

Transcription factors at its regulatory sites (promoter, proximal and distal regulatory sites)

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19
Q

How do stem cells divide? Describe

A
  1. Symmetric self-renewal: From 1 to 2 stem cells (maintains count, extra cell can stay or go)
  2. Asymmetric: From 1 stem cell, to 1 stem cell and 1 progenitor (maintains count, other is committed to differentiation)
  3. Symmetric differentiation: From 1 stem cell, to 2 progenitors (loses count)
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20
Q

In symmetric differentiation, how is the stem cell count maintained?

A

The neighbour has to symmetric self-renew to maintain count

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21
Q

Define:

Progenitor cells

A

Stem cells that have committed to differentiation, cannot go back to the niche

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22
Q

What are the two types of progenitor cells? Explain

A
  1. Multipotent: Upon differentiation
  2. Committed: After further differentiation, they are more differentiated and committed than multipotent
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23
Q

What are the role of stem cells in the body?

A

Maintain tissues in the body
* Epidermal stem cells replenish epithelial skin cells
* Intestinal villi stem cells stay in quiescent stage until transcription factors trigger them to migrate

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24
Q

How is potency of a stem cell tested?

A
  • The unknown stem cells are labeled with fluorescent marker
  • Injected in inner cell mass of blastocyst to form a chimera
  • Implanted into pseudopregnant mouse
  • The offspring is scanned for fluorescent marker
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25
Q

How does the appearance of the marker determine the potency of the stem cell?

A
  • Marker is in wide range of tissue: Pluripotent
  • Marker is in 1 type of tissue: Unipotent
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26
Q

Define:

iPSCs

A

Induced Pluripotent Stem Cells (iPSCs)
* Fibroblasts (obtained easily and non-invasively) that are reprogrammed by adding the 4 Yamanaka factors

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27
Q

What are Yamanaka factors?

A

Transcription factors (TF) that tell the fibroblast to revert to a stem cell

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28
Q

Why are iPSCs very important?

A
  • Very powerful as they can recreate organ systems in vitro without having to get embryonic stem cells
  • More predictable behaviour and easier to culture
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29
Q

List:

The 4 main components of the Lac operon

A
  • Promoter
  • Operator within promoter
  • 3 lac genes
  • Regulatory lacI gene upstream of lac operon
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30
Q

What are the 3 lac genes?

A
  • lacZ: Involved in galactose metabolism, encodes beta-galactosidase
  • lacY: Involved in galactose metabolism, encodes permease
  • lacA
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31
Q

True or False:

The three genes of the operon can be transcribed separately

A

False, as part of an operon, either all 3 genes are transcribed and expressed simultaneously or none are

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32
Q

What does lacI code for?

A

The lac repressor, which binds the operator of the lac operon to suppress expression

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33
Q

How is expression of the lac operon regulated?

A

via transcriptional regulation

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34
Q

Describes:

What happens when lactose is present to the lac operon?

A

The lactose is converted to another form called allolactose, which binds to the lac repressor and inactivates it, meaning it can no longer bind to the promoter and start transcription

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35
Q

What are spliceosomes?

A

Complexes made of snRNPs (protein + RNA) and the pre-mRNA

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36
Q

Where is pre-mRNA cut?

A

5’ and 3’ splice site recognition sequences

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37
Q

What is the 3’ splice site?

A

NCAG

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38
Q

True or False:

Exons are removed, introns are joined together

A

False, the intron is removed, exons are joined together

39
Q

What is abberant mRNA splicing?

A

When one splice site is mutated beyond recognition, and the splice is not correct (may be non-functional as it may contain intronic region)

40
Q

What causes beta-thalassemia?

A
  • Single base substitution
  • Creates new 3’ splice site in the middle of intron
  • Causes some of the intron to be left in the mature mRNA
  • Creates early stop codon, causing much smaller hemoglobin protein to be synthesized
41
Q

What is the basic idea behind beta-thalassemia treatment?

A
  • Using CRISPR Cas9 gene editing
  • Drug is a specific form of fetal hemoglobin
  • Targeting BCL11A, not transcribed meaning that it doesn’t suppress gamma globin gene transcription, cells can produce fetal hemoglobin
42
Q

What is Alzheimer’s disease?

A
  • Progressive and fatal neurodegenerative disease, most common cause of dementia
  • Starts in hippocampus and spreads outwards
  • Loss of neurons, memories and cognitive function
43
Q

Define:

Dendrites

A

Receive signals from surrounding neurons

44
Q

Define:

Soma

A

Cell body with organelles

45
Q

Define:

Axon

A

Long extension of the cell, carries neurotransmitters, nutrients and signals from presynaptic neuron to axon terminal; has myelin sheath

46
Q

Define:

Synaptic cleft

A

Gap where presynaptic neuron axon terminals meet postsynaptic neuron dendrites

47
Q

Define:

Microtubules

A

Essential for nutrient transport and structural support. Stabilized by tau proteins

48
Q

What is the function of cholinergic neurons?

A

Release acetylcholine transmitters (acetyl-CoA + choline)

49
Q

What synthesizes acetylcholine? Where does it do it?

A

Choline acetyl transferase in the neuron

50
Q

What is acetycholinesterase (AChE)?

A

An enzyme on the postsynaptic neuron that degrades acetylcholine back into its components

51
Q

Describe:

The function of acetylcholine in a healthy individual

A
  • Released from the axon terminals of one cholinergic neuron
  • Bind to a receptor on the dendrite of the postsynaptic cholinergic neuron
  • Binding sends out a signal
52
Q

Describe:

Function of acetycholine in patients with AD

A
  • Low levels of choline acetyl transferase (CAT)
  • Pathway is downregulated
53
Q

Why is acetycholine binding to the postsynaptic cholinergic receptor important?

A

Important in initiating a signal cascade

54
Q

What drug is used to treat cholinergic neuron degeneration in AD? Why?

A
  • Acetycholinesterase inhibitors (e.x. rivastigmine)
  • Inhibits the enzyme that breaks down acetycholine, meaning there is more acetycholine around to transmit signal
55
Q

Define:

Amyloid precursor protein (APP)

A

A transmembrane protein that is found in neurons
* Essential in the function, maintenance and repair of neurons
* Not present indefinitely (has lifespan, eventually broken down)

56
Q

List:

The two pathways that APP can be degraded

A
  1. Alpha-secretase + gamma-secretase
  2. Beta-secretase + gamma-secretase
57
Q

Describe:

Alpha + Gamma Secretase degredation pathway for APP

A
  • Cut into small, soluble peptides released into extracellular environment
  • SOLUBLE (cell knows how to deal with this)
  • Dominant degradative pathway
58
Q

Describe:

Beta + Gamma Secretase pathway for APP

A
  • Beta secretase cuts at different locations, released into extracellular environment
  • Produces larger, INSOLUBLE amyloid beta peptide (36-42 amino acids long)
  • Involvement of microglia, astrocytes, and apolipoprotein E are needed to get rid of the amyloid beta peptide
59
Q

Describe:

APP degredation in patients with AD

A
  • More beta secretase than alpha secretase
  • Higher production of insoluble amyloid beta
  • Lower clearance of amyloid beta
  • Leads to plaques
60
Q

How do amyloid beta plaques cause brain deterioration?

A
  1. Excessive release of toxic cytokines leads to inflammatory response, thus neuron loss
  2. Overactivation of microglial cells and astrocytes leads to glutamate build up and neuron damage
  3. Crowded synaptic clefts blocks receptors, leads to decreased communication between neurons
61
Q

What are NMDA antagonists?

A

Inhibit NMDA receptors on the postsynaptic neuron so that excess glutamate has no effect on neurons
* Relieves symptoms, but does not cure disease

62
Q

Define:

Microtubules

A

Key structures of cells (allow molecules/nutrients from stoma to reach axon)

63
Q

Define:

TAU

A

Type of protein that forms subunits in microtubules to hold them together

64
Q

Describe:

TAU and microtubules in AD patients

A
  • TAU protein is hyperphosphorylated
  • Causes TAU protein to dissociate from the microtubule subunits
  • Microtubules then start to fall apart
65
Q

True or False:

If microtubule is non-functional, the cell is mutated but doesn’t die

A

False, the cell dies

66
Q

What happens to hyperphosphorylated TAU proteins?

A

Start to stick to one another, forming intracellular clumps, contributes to cell death

67
Q

What are the clumps formed by hyperphosphorylated TAU proteins known as?

A

Fibrillary tangles

68
Q

What genetic risks increase the chances of AD?

A
  1. Down Syndrome
  2. Presenilin 1 and 2
  3. ApoE4
69
Q

Describe:

Down Syndrome and relation to AD

A
  • Extra chromosome 21 (encodes APP)
  • Higher expression of APP and a much higher risk of early onset AD
70
Q

Describe:

Presenilin 1 and 2, its relation to AD

A
  • Autosomal dominant inheritance
  • Mutant gamma-secretase creates larger amyloid beta peptides (42 aa) leading to greater aggregate production
71
Q

Describe:

Inheritance of ApoE4, its relation to AD

A
  • A less effective variant of ApoE4 that is not effective at removing amyloid beta aggregates
  • High risk of early onset AD
72
Q

What is single cell genome sequencing?

A

The genome of each individual cell within a tumour splice can be sequenced

73
Q

Define:

Intratumoral heterogeneity

A
  • Genetic differences between cells of one tumour in one affected patient
  • A single tumor has multiple patterns of gene expression of different cells
74
Q

Why is intertumoral heterogeneity important?

A
  • Contributes to the complexity of cancer and treatment
  • Precision medicine, takes into account individual cariability in genes, environment, and lifestyle for each person
75
Q

Define:

Intertumoral Heterogeneity

A
  • Between many individuals (even with the same cancer type), you observe differences in gene expression, mutation sequencing
76
Q

Why is intertumoral heterogeneity important?

A
  • Personalized medicine looks at intra-tumoral problems, wondering which mutations exactly to target
77
Q

True or False:

As cells accumulate mutations, the probability of having an oncogenic cell stays the same

A

False, the probability of having an oncogneic cell increases

78
Q

Oncogenic cells will:

A
  • Proliferate
  • Avoid apoptosis
  • Grow
  • Move and invade
  • Create new blood vessels
  • Evade body’s immune response
79
Q

What is the term for creating new blood vessels? What is the purpose of this?

A

Angiogenesis
* To ensure a constant supply of nutrients

80
Q

What are rounds of mutations known as?

A

Clonal expansions

81
Q

Does the order of mutation introduction have an effect?

A

Yes

82
Q

How does clonal evolution and genetic heterogeneity pose an issue to cancer treatment?

A

Which cell mutations should we target?

83
Q

Define:

Passenger mutations

A

Mutations that do not contribute to cancer development, ‘along for the ride’

84
Q

Describe:

Passenger mutations

A
  • Results from normal mutation processes (when DNA divides, endogenous factors)
  • Not really selected for, inert mutations
85
Q

Define:

Driver mutations

A
  • Mutations that contribute to cancer development, and encourages excessive cell growth
86
Q

Describe:

Driver mutations

A
  • First does not cause severe consequence
  • Classified as a mutator phenotype when compuled with a second
  • Third one is early invasive cancer
  • Usually takes 2-5 to get cancer
  • Required for causation, progression, and maintenance of cancer
  • Growth advantage (selected for)
87
Q

What are the two categories of driver mutations (causes of cancer)?

A
  1. Proto-ongenes
  2. Tumour-suppressor genes
88
Q

Why do driver mutations tend to be in proto-oncogenes and tumour-suppressor genes?

A

They are more likely to lead to cancer progression

89
Q

What are proto-oncogenes?

A

Genes involved in promoting cell survival, growth, and movement
* Mutations in genes are likely to lead to oncogenic phenotypes (e.x. growth factors)

90
Q

In proto-oncogenes, what does a mutation imply?

A

Gain of function: Pathway is overexpressed, cancer cells can induce receptor to be constitutively active

91
Q

Give an example of a growth factor receptor

A

Receptor Tyrosine Kinase (RTK), which binds to growth factor, activating a transcription factor that will bind to promoter/regulatory regions; activating expression genes necessary for cell growth

92
Q

What are tumour suppresor genes? What happens when they mutate?

A

Genes that are involved ins topping cell cyle, inducing apoptosis, recognizing DNA damage
* Mutations causes loss of regulation of cell cycle

93
Q

What is the most common mutation involving tumor suppressing gene?

A

P53 (over 60% of cancers involve this mutation)
* Mutations in the DNA binding domain region of P53 hinders ability to be a transcription factor

94
Q

What are cancer stem cells?

A
  • Slowly dividing cancer cells
  • Resistant to chemotherapy
  • Results in tumour lapse

My Packs: UWO (BIO 1002) (10 decks)

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