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DEN203 > G&D- Cells > Flashcards

G&D- Cells Flashcards

1
Q

What % of genome is translated into proteins?

A

3%

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2
Q

What % of genome is transcribed as part of protein-coding gene expression but not translated into proteins?

A

27%

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3
Q

What % of genome is transcribed and not translated AND is not associated with protein-coding gene expression…?

A

25%

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4
Q

How many non-functional pseudogenes in the genome?

A

20,000

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5
Q

What is a pseudogene?

A

Section of chromosome that is an imperfect copy of a functional gene.

  • Related to real genes
  • Contain biological and evolutionary histories
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6
Q

What are the 4 nucleobases in DNA?

A
  • Adenine
  • Thymine
  • Guanine
  • Cytosine
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7
Q

RNA nucleobases?

A
  • Adenine
  • Uracil
    Guanine
    Cytosine
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8
Q

What is transcription?

A

Process by which gene information from DNA strand is transferred to an RNA molecule… genetic information is now on the coding strand!
This mRNA molecule is complimentary to the DNA template strand!

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9
Q

What is RNA polymerase?

A

Protein that binds onto the promoter sequence on an DNA template strand sequence to begin transcription.
- No primer required

Polymerase 2- used for mRNA precursors

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10
Q

How might translocation mutations of enhancers and promoters lead to cancer?

A

Translocation may place genes that should be turned off in proximity of strong promoters and enhancers- these control transcription rates and gene expression (timing and in which specific cell types!)

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11
Q

What is the 3’ strand?

A

Coding strand

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12
Q

What is the 5’ strand?

A

Template strand

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13
Q

What is pre-mRNA?

A

Type of primary transcript that becomes mRNA after processing (alternative splicing- removing non-coding introns with a splicesome)

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14
Q

What is mRNA?

A

Wide range of sizes depending on polypeptide size.

Common to most cells- proteins needed by all cells.

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15
Q

What is rRNA?

A

Builds ribosomes, machinery for synthesising proteins by translating mRNA…
4 kinds in eukaryotes: 18s, 28s, 5.8s, 5s
s= sedementation rate

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16
Q

What is tRNA?

A

32 different kinds in eukaryote cells…
- Carries AAs (1/20) at the 3’ end
Most AAs have more than 1 tRNA

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17
Q

What is ncRNA

A

non-coding RNA
2% of genome.
90% of genome is transcribed.
- Modify protein levels by mechanisms independent of transcription…
- ncRNA: plays a role in cellular physiology, development, metabolism
- Epigenetic modulator

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18
Q

snRNA

A

Small nuclear RNA
Mediate processing steps of precursor molecules/primary transcripts before they can be exported into cytosol…
- Part of splicesome?

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19
Q

snoRNA

A

small nucleolar RNA
Help make ribosomes by helping cut large precursors.
- Can add methly groups to ribose
- Involved in splicing of pre-mRNA

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20
Q

What are microRNAs?

A

Tiny RNA molecules
- Regulate gene function post-transcriptionally
- Account for 1/3 of protein-coding genes
- Bind to mRNA, cause degradation/ inhibit protein syntehsis
18-25 nucleotides
- Time specific expression!

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21
Q

Name 3 energy yielding nutrients

From diet

A

Fats
Carbohydrates
Proteins

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22
Q

Name 3 energy-poor, end-products (made through catabolism of energy-high products)

A

H2O
CO2
NH3

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23
Q

Name some precursor molecules for cell macromolecules… (4)

A
  • AAs
  • Sugars
  • Fatty acids
  • Nitrogenous bases
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24
Q

Name 4 cell macromolecules made through anabolism of precursor molecules

A
  • Nucleic acids
    Proteins
    Lipids
    Polysaccharides
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25
Q

Name the 2 types of protein (turnover) regulation

A

Allosteric

Transcriptional

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26
Q

What are the 3 types of AAs?

A
  • Essential; from diet

(synthesised in body)

  • Non-essential
  • Conditionally essential AAs
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27
Q

What are essential AAs?

A 
From diet only.
9 
1- histidine
2- isoleucine
3- leucine
4- lysine
5- methionine
6- phenylalanine
7- threonine
8- typtophan
9- valine
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28
Q

What are non-essential AAs?

A 
Synthesised in body
Can be made from:
- Glucose + Nitrogen source 
or...
- Made from the essential AAs
5
1- alanine
2- aspargine
3- glutamate
4- asparate
5- serine
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29
Q

What are Conditionally essential AAs?

A

Synthesised in body (6)
Can be synthesised bu may not be enough i.e….
Arginine is essential during period of rapid growth so must be supplement throughout this period as cannot be made fast enough.

1-  Arginine
2- cysteine
3- glutamine
4- glycine
5- proline
6- tyrosine
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30
Q

How many standard and non-standard AAs are there?

A

S- 20

Non-s : 2

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31
Q

What are the 2 non-standard AAs?

A

1) Selenocysteine: Found on prokaryotes, eukaryotes too but not loaded by DNA?
2) Pyrolysine: found only in some archaea and bacteriu

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32
Q

2 types of AAs (in relation to how they are degraded/ where the carbons go to…)

A

1- Glucogenic: carbons are converted to glucose
2- Ketogenic: Carbons are converted to acetyl CoA or Acetoacetate (ketone bodies)

Some are both!

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33
Q

Where does amino acid degradation occur?

A

Liver

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34
Q

Where does the carbon and where does the nitrogen go?

A

Carbon: Glucose, CO2 , acetyl CoA, acetoacetate

Nitrogen:
Alpha amino group is removed; ammonia is formed which enters the urea cycle.

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35
Q

What is transamination?

A

When an amino group from one amino acid is transferred to another.

e.g. α ketoglutarate and glutamate are usually one pair

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36
Q

What enzyme and co-factors are needed for transamination?

A

transaminases/amino transferases

Cofactor- pyridoxyl phosphate (derived from vit. B6 )

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37
Q

How is ammonia produced from AAs?

Enzyme involved?

Where?

A

Glutamate can collect nitrogen from AAs and convert it to Ammonia…

Glutamate dehydrogenase

Liver mitochondria

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38
Q

Protein degradation intracellular-

A

Lysosomes: vesicles filled with protease

Ubiquitin: small proteins that targets proteins for degradation

Proteasome: protease complex, protein is unfolded & degraded (ATP)

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39
Q

Nitrogen

A

N2 not usable in biological systems

NH3, usable & crosses membranes

NH4+ toxic

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40
Q

Forms of nitrogen that are excreted

A

Ammonia
Uric acid
Urea

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41
Q

Who may have a positive nitrogen balance (above normal)?

A

Children

Pregnant

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42
Q

Who may have a -ive N balance?

A

Disease

Starvation

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43
Q

Urea cycle

A

5 steps.

Nitrogen enters as NH4+ and aspartate

Ornithine initiates and is regenerated.

Enzyme mediated

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44
Q

Control of urea cycle?

A

1- ‘Feed forward’ regulation: the higher the rate of ammonia production the higher the rate of urea

2- Allosteric activation of enzymes
(arginine stimulates carbamoyl phosphate synthase)

3- High protein diet or fasting induces urea cycle enzymes

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45
Q

What happens in muscles during fasting?

A

Muscle protein broken down to amino acids…

Pyruvate-> Alanine
Alanine (AA) and glutamine (mops up nitrogen) enter blood…

These AAs are broken down to (-> Pyruvate -> ) glucose and ketone bodies in the liver and used for energy!

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46
Q

What are ketone bodies?

A

Acetoacetate, beta hydroxybutyrate
- acidic

3 water-soluble molecuels containing the ketone group.

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47
Q

When glucose low, what happens to ketone bodies?

A

Acetoacetate, beta hydroxybutyrate

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48
Q

ketoacidosis?

A

Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids

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49
Q

What are some Inborn errors of amino acid metabolism?

A

Deficient enzymes in amino acid metabolism lead to accumulation of harmful products

Phenylketonuria: mutation in phenylalanine hydroxylase, mental retardation

Urea cycle disorders: accumulation of ammonia, toxic to the nervous system

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50
Q

What is Phenylketonuria?

A

mental retardation

mutation in phenylalanine hydroxylase

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51
Q

How are Non essential amino acids made

A

synthesised from intermediates of glycolysis and the TCA cycle

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52
Q

Where do the carbons in AAs go when AAs are degraded?

A

the carbons from amino acids form glucose or acetyl CoA/acetoacetate

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53
Q

Where do the nitrogens in AAs go when AAs are degraded?

A

Nitrogen is removed by transamination, formation of ammonia and formation of urea in the urea cycle

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54
Q

Functions of Cell communication?

A

adaptation,
co-ordination
and regulation

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55
Q

3 mechanisms of cell communication ?

A
  1. Remote signalling by
    Secreted molecules
  2. Contact signalling by
    membrane bound
    molecules
  3. Contact signalling via
    Gap junctions
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56
Q
  1. Remote signalling by
    Secreted molecules

e.g. Chemical signalling (secreted)

4 mechanisms..

A

1- Endocrine
2- Paracrine
3- Autocrine
4- Synaptic

57
Q

What is endocrine signalling?

A

Hormones

hormone produced, enters bloodstream and is carried to target cell.

58
Q

What is paracrine signalling?

A

local chemical mediator released, acts on cells in immediate environment

(eg cytokine)

59
Q

What is autocrine signalling?

A

Acts on itself

60
Q

What is synaptic signalling?

A

neurotransmitters released at synapses, diffuse to post-synaptic target cell.

61
Q

Examples of signals

A 
Growth factors (hormones, endocrines)
 Hormones
 Extra-cellular matrix (can be insoluble)
 Chemicals
 Proteins
 Sugars
 Synaptic
62
Q

Examples of cell responses to signals

A 
Growth, cell division
Differentiation
Metabolism
Apoptosis
Gene transcription- start and stop
Secretion
Contract / relax- muscle cell
Membrane charge
Migration- chemokine/cytokine, move along conc gradient
63
Q

Signal Transduction mechanisms (3)

A

Amplification,

phosphorylation cascades,

secondary messengers

64
Q

Intracellular receptors- mechanism

A

Hydrophobic molecules– can pass through plasma membrane

Transported into nucleus

Response: influence gene transcription

65
Q

Name some substances that may act on intracellular receptors

A

eg Steroids,

NO- nitrous oxide

66
Q

What is Phosphorylation

A

Proteins can be modified… by phosphorylating

Any enzyme that is a kinase, sticks a phosphate on a protein

67
Q

Name 4 membrane receptors

A

G-protein linked
Tyrosine kinases
Enzyme linked
Ion channels

68
Q

What are G-protein coupled receptors

?

A

Integral trans-membrane proteins

Receptor occupation promotes interaction with G-protein

Promotes exchange of bound GDP -> GTP… activates G protein (α subunit) which leaves receptor

… initiates signalling through secondary messengers

69
Q

What are Monomeric (small) G-proteins: Ras?

A

Function controlled by GDP/GTP cycle.

Stimulates cascade of kinases (effectors).

Involved in Proliferation, differentiation, cell death

70
Q

Mutations in Ras proteins?

A

Mutations make Ras insensitive to GTPase activating proteins (active for longer).
Ras mutations in 30% of all tumours.

Cancerous!

71
Q

Receptor tyrosine kinase mechanism- …

A

Ligand binds.
Dimerise upon ligand binding.

Have intrinsic enzymatic activity.

Phosphate from ATP to tyrosine on itself (autophsophorylation).

Bind src homology-2 (SH-2) proteins.

Initiate series of phosphorylation reactions

72
Q

What does MAP stand for?

A

Mitogen activated protein (MAP) kinase system

cascade trasnduction…
Phosphylation cascade…

73
Q

What are enzyme-linked receptors?

A

Cytokine receptors – no intrinsic activity but associates with enzymes

e.g. JAKs

cytokine binds; dimerise reaction…

74
Q

What are ion channels?

A

Ion channel= receptor.

Ligand (eg neurotransmitter) binds to& opens channel (some are voltage gated)

Response: influx of Na+, change in membrane potential, action potential

75
Q

What are secondary messengers?

A

Small molecules

Bind and activates other molecules

76
Q

Examples of 2ndary messengers

A

Cyclic adensosine monophosphate (cAMP)
Inositol triphosphate (IP3)
Ca2+ - (muscle contraction)
Diacylglycerol

77
Q

What are kinases/ phosphatases?

A

A kinase is an enzyme that attaches a phosphate group to a protein. A phosphatase is an enzyme that removes a phosphate group from a protein.

Together, these two families of enzymes act to modulate the activities of the proteins in a cell, often in response to external stimuli.

78
Q

How is control of signalling?

A

Inhibition by protein phosphatases

79
Q

Fibroblast growth factor receptor (FGFR) stimulation- what diff effects does it have on differing cell types…?

A

1) in fibroblasts - proliferation

2) in neuronal cells – differentiation

80
Q

PD184352 (MEK) function?

A

Specific inhibitors - PD184352 (MEK) reduce tumour growth by up to 80%

81
Q

What is PTEN?

A

PTEN is a tumour suppressor and is a IP3 phosphatase

82
Q

Overexpression of what cell signals in cancer?

A

MAPK, PI3K

Activating mutations of G subunits & receptors
????

83
Q

Therapeutic caner targets…

News: Experimental Drug Inhibits Cell Signaling Pathway and Slows Ovarian Cancer Growth

Trying to affect cancer cell signalling pathways… to inhibit growth

A

targeted agents currently under development interfere with function and expression of several signalling molecules,

including the EGFR family;
the vascular endothelial growth factor and its receptors;

and cytoplasmic kinases such as Ras, PI3K and mTOR

84
Q

What are VNTRs?

A

“Variable number tandem repeats”

Repeat nucleotide regions usually bounded by specific restriction enzyme sites,
> Number of repeats at each loci is inherited from parents

30% non-coding region

There is large variation between people…

85
Q

PCR and DNA amplification use?

A

Measuring transcription of a gene…

86
Q

What is reverse transcription?

A

Using RNA to make cDNA and then using polymerase chain reaction to make more copies of a specific piece of DNA

  • Once you have lots of DNa copies, can identify defect
87
Q

3 steps of PCR

A

1- Denaturation
2- Annealing
3- Extension

88
Q

What are SNPs

A

Single Nucleotide polymorphism

DNA sequence variation: when a single nucleotide in genome sequence has been altered!
Most commonly: C-> T

89
Q

What % of all genetic variaton occurs due to SNPs

A

90%

Has to occur in at least 1% of population

90
Q

What is the cell cycle?

A

Ordered set of events that leads to cell growth and division.
Involves mitosis.

91
Q

What is mitosis?

A

Production of 2 identical daughter cells.

- DNA is duplicated exactly and divided equally. (complete set in daughter cells)

92
Q

What is miosis?

A

Division that leads to gamete formation.

93
Q

What happens in gap1 (8-10hrs)

A

Cell grows: it is metabollically active

- duplicates organelles (excluding chromosomes)

94
Q

What happens in S phase?

6-8hrs

A

“interphase”

Replication of DNA… there is now 46 chromosomes

95
Q

What happens in gap 2 phase?

4-6hrs

A

Cell growth continues… as it prepares to divide.
Enzymes and other proteins are synthesised.
Double checks for errors are done in this phase too.

96
Q

What happens during mitosis?

A

Cell division occurs!

  • Prophase
  • Metaphase
  • Anaphase
  • Telophase
    + Cytokenesis
97
Q

Gap 0 phase?

A

Exit from cell cycle- for non-dividing cells

98
Q

What happens in interphase?

A

Chromosomes duplicate, thicken and coil

99
Q

What happens in prophase?

A

Nuclear membrane breaks down

100
Q

What happens in metaphase?

A

Centromeres attach to spindle fibres and line up at the equator

101
Q

What happens in anaphase?

A

Centromeres split and are pulled to each half of the cell

102
Q

What happens in telophase?

A

Cytokenesis occurs. cells are pulled apart.

- Nuclear membranes form around the separated chromosomes.

103
Q

Name 3 cell cycle regulation checks

A

G1 checkppoint- Growth and environment
G2 checkpoint- DNA replication
M checkpoint- Chromosome alignment on spindle

104
Q

What are cyclins?

A

family of regulatory proteins that control the progression of cells through the cell cycle by activating cyclin-dependent kinase (CDK) enzymes.

Levels rise and fall within stages of the cell cycle

105
Q

Cyclins present in G1 phase

A

D

106
Q

Cyclins present in S phase

A

D?, E and A

107
Q

Cyclins present in M phase

A

D?, B and A

108
Q

What are Cyclin dependent kinases (Cdks)

A

Enzymes that Trigger major cell cycle transitions
via: Phosphorylate proteins that control cell cycle

-> Activity controlled by Cdk inhibitors

109
Q

Cyclin dependent kinases (Cdks) bind to which cyclin…

in G1 phase!!

A

Cdk4 & 6 D Cyclin

110
Q

Cyclin dependent kinases (Cdks) bind to which cyclin…

in G1 to S phase!!

A

Cdk 2 E Cyclin

111
Q

Cyclin dependent kinases (Cdks) bind to which cyclin…

in s phase!!

A

Cdk2 A Cyclin

112
Q

Cyclin dependent kinases (Cdks) bind to which cyclin…

in S to G2 phase!!

A

Cdk1 A Cyclin

113
Q

Cyclin dependent kinases (Cdks) bind to which cyclin…

in M phase!!

A

Cdk1 B Cyclin

114
Q

What is MPF?

A

Mitosis promoting Factor (MPF)… initiates mitosis

  • Activates anaphase promoting factor/ anaphase
115
Q

What is the G0 phase?

A

Quiescent cells that have permanently or temporally left the cell cycle e.g. lymphocyte.

116
Q

Why might a cell enter the G0 phase?

A

Terminal differentiation e.g. neuron, epithelial cell.

Active repression of genes needed for cell cycle.

117
Q

What is the p53 gene?

A

cell cycle regulatory genes
also a tumour suppressor genes

p53 blocks cell cycle if DNA is damaged.
- Mutated in approx. 50% of cancers

118
Q

p27 cyclin dependent kinase inhibitor… reduced levels can lead to…

A

poor breast cancer outcomes?

119
Q

What is apoptosis?

A

Programmed cell death, essential for normal development.

120
Q

3 functions for apoptosis

A

1) destroys cells that may be a threat:
- virus infected, immune, DNA damage

2) withdraw of positive signals
eg growth factors, hormones

3) receipt of negative signals
eg UV, death activators, hypoxia

121
Q

Features of apoptosis…

A 
> Controlled
> Energy dependent
> Cells shrink
> Membrane intact
> Non-inflammatory
> No scarring
> No individual or small cell groups
> Nuclear fragmentation
> Physiological (or pathalogical)
122
Q

Features of Necrosis…

A 
> Uncontrolled
> No ATP required
> Cells swell
> No membrane integrity
> Inflammatory
> Scarring
> Large cell groups
> Nuclear dissolution
> Pathological
123
Q

2 main pathways that tell a cell to die…

A

1- intrinsic: integrity of mitochondrian membrane- cytochrome C release into cytoplasm… binds to Apaf-1 protein… there is a cascade of enzyme reactions

2- extrinsic: ligand binding to ‘death receptors’… there is a cascade of ‘caspase activation’… apoptosis…

124
Q

What are caspases?

Key players: Bcl-2, Fas/L, Caspases

A

Proteolytic enzymes… cystein proteases

Effectors of apoptosis…
- Present as inactive proenzymes (zymogen)

125
Q

Apoptosis examples in dental physiology?

A 
Craniofacial growth & development
Homeostasis in mucosa, skin & pulp
Tooth development
Bone remodelling
Wound healing
126
Q

Apoptosis in disease examples?

A

Avoidance in cancer = survival/proliferation

Human Papilloma virus inactivates p53
Epstein Barr Virus protein similar to Bcl-2
Melanoma inhibits expression of Apaf-1
Fas antagonists – block T cell cytotoxicity
Autoimmune eg SLE, Rheumatoid arthritis

Increase in apoptosis
eg Neurodegenerative, HIV

127
Q

Apoptosis in oral disease

A

Oral cancer
Lymphomas- reduced apop
Odontogenic tumours/cysts
Sjogren’s syndrome

128
Q

Apoptosis in oral pathology

A

Common in Lichen planus?= chronic inflammatory dematosis… keratinocyte apoptosis

129
Q

What are pluripotent cells?

A

Can diff into Any type of cell in the adult

e.g. Embryonic

130
Q

What are multipotent cells?

A

Limited diff, found in bone marrow and most organs

131
Q

What is SHED?

A

Stem cells from human exfoliated deciduous teeth (SHED):

multipotent, capable of differentiating into neural cells, odontoblasts.

132
Q

Dental applications of SHED

A
  • Growing teeth
  • Repair/regeneration of dental tissues… e.g. pulp/ pdl
  • Craniomaxillofacial bone repair
133
Q

Problems with stem cells

A
  • Rejection/ immune reaction
  • Legal, ethical, political issues
  • Adult stem cells difficult to isolate and purify
  • May result in cancer
134
Q

What is gene therapy?

A

Correcting defective genes responsible for disease development

Vector: commonly viruses; e.g. retro, adeno, adeno-associated

135
Q

What is salivary gland gene therapy?

A

S.glands are encapsulated and accesible.

  • Stable cell populaiton which export a large amount of proteins
  • Can be removed if problem arises…
  • Sjogren’s syndrome… radiation damage…
  • Systemic conditions
136
Q

What is epigenetics?

A

Heritable phenotype resulting from changes in a chromosome without alterations in the DNA sequence (IVF)

  • Identical DNA, but diff terminal phenotypes
137
Q

how does epigenetics occur?

A
  • DNA methylation
  • Histone modification
  • Nucleosome modification
  • non coding DNA (micro DNA)
138
Q

What are exosomes?

A

Durable cell specific lipid microvesicles…

  • Reside in a number of biofluids
  • Have immune functions

DEN203 (11 decks)

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