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I&I WC1 > Intracellular processes > Flashcards

Intracellular processes Flashcards

1
Q

What is epigenetics?

A

Changes in phenotype, without changes in genotype -> by regulation of expression

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2
Q

Epigenetic changes can come about as a result of influences from the environment. When is the effect of influences from the environment greatest?

A

If they occur early in gestation

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3
Q

What is lyonization?

A

X-inactivation in females

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4
Q

What are housekeeping genes?

A

Genes needed by (nearly) all cells

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5
Q

What is a nucleosome?

A

DNA wrapped around histones

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6
Q

How many types of histone are there?

A

4

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7
Q

What is the effect of DNA being wrapped around nucleosomes?

A

It is less accessible to transcription factors and transcription machinery

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8
Q

What are the two key players in regulating gene transcription?

A
  1. Transcription factors
  2. Gene regulatory elements
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9
Q

Which epigenetic mechanisms does the body have to regulate gene transcription? (4)

A
  1. DNA methylation
  2. Nucleosome positioning
  3. Histone modifications
  4. 3D genome folding
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10
Q

In which way are epigenetic modifications related to immunological memory?

A

After immune cells have been activated, epigenetic changes remain that allow them to quicker upregulate immunological functions -> allows for quick response

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11
Q

What are gene regulatory elements?

A

Short stretches of DNA with certain motifs, to which transcription factors can bind

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12
Q

In which two groups can gene regulatory elements be divided, based on proximity to the gene they regulate?

A
  1. Close to the transcription start site (=promotor)
  2. Distal to the transcription start site
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13
Q

Which gene regulatory elements can be found distal to the transcription start site? (4)

A
  1. Enhancer
  2. Silencer
  3. Insulator
  4. Locus control regions
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14
Q

What is an enhancer?

A

Sequence of non-coding DNA that enhances formation of transcriptional loops

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15
Q

What is a silencer?

A

A repressor of transcription activation

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16
Q

What is an insulator?

A

A gene regulatory element that prevents transcriptional looping

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17
Q

What is a locus control region?

A

A group of enhancers that work together, often in a cluster of genes

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18
Q

What is an example of genes which are modulated by a locus control region?

A

Cytokine genes

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19
Q

How are transcription factors (often) activated?

A

Signalling cascades, often from receptors

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20
Q

How can distal gene regulatory elements influence DNA activity if DNA is linear?

A

DNA is not linear, but rather folded and curled, allowing for the formation of transcriptional loops

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21
Q

What is the function of transcription factor Pax5? What happens when it is absent?

A

Needed by B-cells to differentiate and maintain B-cell phenotype

In abcence of Pax5, B-cells will differentiate into different phenotypes depending on environmental signals

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22
Q

True or false: after a cell has differentiated into a specific phenotype, it no longer needs its cell-type specific transcription factors

A

False; cells need their transcription factors to maintain their phenotype

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23
Q

What are mechanisms and mutations in epigenetic regulation that can lead to disease? (4)

A
  1. Mutation of regulators can block their binding to gene regulatory elements
  2. Fusion of regulators can lead to dysfunctional binding to enhancers
  3. Mutations in GRE-sequences in DNA can block (complete) binding of regulators
  4. Mutations in DNA sequence of GREs can weaken/strengthen binding of regulators -> phenotypic variation of gene activity
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24
Q

True or false: mutations in the GREs often cause complete blockage of the binding of regulators to GREs

A

False; often there is only partially decreased activity of regulator and not complete failure

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25
Q

What can be the effects of phenotypic variation of gene activity caused by mutations in DNA-motifs of GREs leading to stronger/weaker binding of regulators? (3)

A
  1. Non-harmful phenotypic variations
  2. Higher susceptibility to disease
  3. Disease
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26
Q

What is DNA methylation? Which nucleotide is methylated?

A

Coupling of a methyl group to cytosine

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27
Q

Which enyzme methylates DNA?

A

DNA methyl transferase (DNMT)

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28
Q

Which enzyme demethylates DNA?

A

TET

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29
Q

What is the effect of DNA methylation? (2)

A
  1. Prevention of TF binding by blocking enhancer/promotor, causing genes to be silenced
  2. Recruitment of repressor molecules, causing genes to be silenced
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30
Q

What is the source of methyl groups of DNA methylation?

A

Folic acid

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31
Q

What is genomic imprinting?

A

An epigenetic regulatory mechanism in which only either the maternal or paternal gene is expressed, and the other one is shut down

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32
Q

How many genes use genomic imprinting?

A

<100

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33
Q

What is the effect of loss of genomic imprinting?

A

Often not compatible with life, and otherwise leading to severe syndromes

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34
Q

By which two ways can disrupted methylation lead to oncological processes?

A
  1. Methylation of tumorsuppressor genes
  2. Demethylation of oncogenes
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35
Q

How does nucleosome positioning dictate gene transcription?

A

Nucleosomes prevent transcription factors from binding -> positions of nucleosomes can make genes more/less accessible

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36
Q

How do chromatin remodelers change the accessibility of DNA? (2)

A
  1. Sliding nucleosomes to create space for transcription factor binding
  2. Assembling/disassembling nucleosomes
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37
Q

What are histone modifications?

A

Addition of groups to histone tails, influencing how tightly DNA is bound around nucleosomes

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38
Q

What is the most important kind of histone modification?

A

Acetylation

39
Q

Closed chromatin has a [low/high] amount of acetyl groups as histone modifications, whereas open chromatin has a [low/high] amount of acetyl groups

A

Closed chromatin = low acetylation
Open chromatin = high acetylation

40
Q

Which enzyme adds acetyl groups to histones?

A

HAT

41
Q

Which enzyme removes acetyl groups from histones?

A

HDAC

42
Q

By which mechanism do histone modifications influence how tightly DNA is bound around nucleosomes and the accesibility of DNA for transcription factors? (2)

A
  1. Histone modifications impact charge of DNA
  2. Histone modifications can lead to steric hindrance
43
Q

True or false: one histone tail can only have one modification

A

False; histone tails can have multiple modifications

44
Q

True or false: silencing by DNA methylation is usually also associated by deacetylated histones

A

True

45
Q

What is the chromatin configuration of the cytokine genes in memory T-cells?

A

Open configuration -> readily accessible for rapid respoonse

46
Q

How can DNA methylation/modifications be identified?

A

Induce DNA breaks and incubate DNA with antibodies that recognize specific modifications to fish these fragments out. Fragments are then mapped back to the genome

47
Q

What is Tn5? How can it be used to show DNA binding around nucleosomes?

A

An enzyme that wants to cut DNA at every possible site. Cannot cut histone-bound DNA -> these fragments can be fished out and mapped back to the genome

48
Q

What is bisulfite sequencing? How can it be used to identify methylation patterns?

A

It causes unmethylated C to turn into U -> can be sequenced and mapped back to the genome

49
Q

What is the most common method of DNA folding?

A

DNA looping

50
Q

What is the approximate size of DNA loops? What is the area inside this loop called?

A

~200.000 base pairs; area inside this loop = contact domain

51
Q

How are DNA loops created?

A

Created by various proteins that recognize DNA motifs

52
Q

What is often a common characteristic of genes within the same contact domain created by DNA folding?

A

Often have the same epigenetic characteristics -> all turned on or off

53
Q

What are nuclear subcompartments? What is their function?

A

Compartments within the nucleus that contain contact domains with comparable activity -> active and inactive regions grouped, allowing for efficient concentration of transcription machinery, nucleic acids, etc.

54
Q

What is an important function of DNA function in VDJ-recombination?

A

It ensures that all V-genes are equally close to the recombination centre, giving all V-genes an equal chance to be incorporated

55
Q

Which epigenetic change is most often used as a biomarker?

A

Methylation

56
Q

What is an example of drugs that are used to modify epigenetics? What is their effect?

A

BET-inhibitors -> alter DNA methylation

57
Q

What is the problem in using drugs that target epigenetic modifications?

A

Aspecific -> epigenetic profile of all cells altered, causing side effects

58
Q

What is signal transduction (definition)?

A

Any process by which a cell converts one kind of signal/stimulus into another, involving ordered sequences of biochemical reactions inside the cell

59
Q

What is the prototypic basic signalling cascade? (4)

A
  1. Ligand activates receptor
  2. Receptor activates protein at membrane
  3. Protein at membrane activates protein in cytosol
  4. Protein in scytosol = activated final target of pathway, leading to a response
60
Q

What are two common locations of ligand binding receptors?

A
  1. Cell surface
  2. Intracellularly, such as in endosomes
61
Q

Which groups of proteins are often involved in signal transduction? (4)

A
  1. Linkers/adaptors
  2. Kinases/phosphatases
  3. Lipid-metabolizing enzymes
  4. Guanine nucleotide exchange factors (GTP/GDP)
62
Q

What are linkers/adaptors?

A

Building bocks that interact with other signaling molecules, without having enzymatic activity themselves

63
Q

How do signaling proteins interact with one another?

A

Via modular protein domains

64
Q

Where are the first intracellular signaling proteins in a signaling cascade often found?

A

Bound to the plasma membrane

65
Q

What are ways in which signaling molecules can be recruited to the plasma membrane? (3)

A
  1. Binding to phosphorylated sites on membrane-associated proteins
  2. Being recruited by RAS-proteins
  3. Binding to membrane lipids
66
Q

How can phosphorylation lead to recruitment of signaling molecules?

A

By providing a docking site for these signaling molecules

67
Q

What are RAS-proteins, and how are they activated?

A

Plasma-membrane bound proteins that are activated through confirmational changes when a linked receptor is activated -> provides docking sites for intracellular proteins

68
Q

Which two types of linkers can be identified?

A
  1. Scaffolds
  2. Adaptors
69
Q

What are scaffolds?

A

Proteins without enzymatic activity that can function as a docking site for other proteins

70
Q

How are docking sites created on scaffolds?

A

Phosphorylation

71
Q

What are adaptors?

A

Proteins that don’t require phosphorylation and can directly connect to other signaling proteins

72
Q

True or false: phosphorylation leads to activation, whereas dephosphorylation leads to deactivation

A

False; this is not always necessarily the case

73
Q

How can signaling proteins be involved in multiple pathways?

A

Having multiple phosphorylation sites with different functions

74
Q

What is a common method of intracellular signaling amplification?

A

Kinase cascades

75
Q

What is a second messenger?

A

Soluble messenger inside the cell

76
Q

What are common second messengers? (2)

A
  1. Calcium
  2. cAMP
77
Q

What is the function of calcium and cAMP as seond messengers?

A

Rapidly diffuse throughout the cell and induce confirmational changes in calmodulin

78
Q

Why are calcium and cAMP good second messengers?

A

They can be rapidly produced (cAMP) or released (calcium) upon activation

79
Q

Why is intracellular signal amplification necessary in (most) signaling cascades?

A

Allows for a robust signal, even when little ligand is present

80
Q

What are the three general outcomes of signaling pathways?

A
  1. Alterations in gene transcription
  2. Cytoskeleton changes, leading to migration
  3. Alterations in cell metabolism
81
Q

What are three common methods to switch off cellular signaling cascades? (3)

A
  1. Altering phosphorylation
  2. Ubiquitin-mediated degradation in proteasome
  3. Ubiquitin-mediated degradation in lysosome
82
Q

What is a characteristic that the BCR and TCR share when it comes to signaling?

A

They don’t have an intracellular domain, requiring signal transducers

83
Q

What are the signal transducers of the BCR?

A

Igα-Igβ

84
Q

Which BCR is an exception to the rule that BCR’s dont have a signaling domain? What is the effect of this?

A

IgG-receptor -> IgG can bypass signaling steps, allowing for a quicker response

85
Q

What is the signal transducer of the TCR?

A

CD3

86
Q

Why do drugs that interfere with the TCR often also have (some) effect on BCR signaling (and vice versa)?

A

They use a very similar signal transduction pathway

87
Q

What is the shortest known signaling cascasde in immune signaling? What are its steps? (4)

A

Cytokine signaling through JAK-STAT

  1. Binding of cytokine leads to receptor dimerization
  2. Dimerization leads to JAK activation
  3. Activated JAKs activate STAT through phosphorylation
  4. STAT activates transcriptoin
88
Q

Why do defects in (immune) signaling pathways (often) not immediately lead to disease?

A

Most signaling pathways have redundancy

89
Q

How can targeting Notch signaling to combat T-cell leukaemia lead to skin problems?

A

While Notch signaling is important for T-cell proliferation, it is also important for protection against cancer in the skin

90
Q

What are the effects of:
1. No BTK signaling
2. Permanent BTK activation
3. Increase of BTK protein

A
  1. No signaling = no development of B-cells -> XLA
  2. Permanent activation = constant B-cell stimulation -> CLL
  3. Increased = higher survival of autoreactive B-cells -> spontaneous auto-immune phenotype
91
Q

How can targeting of BTK kill CLL cells?

A

BTK inhibitors block CXCR4 chemokine signaling in B-cells -> CLL cells enter circulation, where they die

92
Q

After some time of using BTK inhibitors, cells will lose their susceptibility to this class of drugs. Why?

A

Their pathways rewire in a way does not require BTK -> shows redundancy

93
Q

How can phosphorylation of signaling proteins be measured? (2)

A
  1. Western Blot -> bulk
  2. Phosphoflow -> cell-specific

I&I WC1 (20 decks)

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