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Molecular Genetics > Exam II (lecture 9-13) > Flashcards

Exam II (lecture 9-13) Flashcards

1
Q

Eukaryotic nuclear chromosomes

A

Chromosoomes are linear and usually very long
- many origins per chromosomes
- slower replication
- shorter okazaki fragments

Histones
Centrpmeres
Linear chromosomes have “end replication problem”

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2
Q

DNA replication takes place during what phase?

A

S phase, which is part of the interphase of the cell cycle.

Two identical chromosomes are produced, attached at the centromer

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3
Q

Yeast origin

A

ARS (autonomous replicating sequence)

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4
Q

Creating replication forks at ARS

A
  1. origin selection - formation of prereplicative complex (pre-RC) during G1 of cell cycle
  2. Origin activation - at the beginning of S phase
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5
Q

Step 1 origin selection:

A
  1. origin (or replicator) - ARS (in yeast) (autonomously replicating sequence
  2. Eukaryotic initator - heteohexamer ORC (origin recognition complex)
  3. ORC - (trans acting factors) recognize and bind to ARSs (cis acting elements). ATP is required for ORC binding.
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6
Q

ORC vs ARS

A

ORC - trans acting factors
ARS - cis acting elements

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7
Q

Formation of a prereplication complex (pre-RC) in G1.

A
  1. binding of initator (ORC)
  2. Binding of helicase loaders (Cdc6 and Cdt1)
  3. “Loading of helicases” (Mcm2-7)
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8
Q

Pre-RC consists of

A

ORC, Cdc6, Cdt1, Mcm2-7

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9
Q

Formation and activation of preRC is controlled by

A

Cdk (cyclin dependent kinase)

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10
Q

PreRC (origin) activation

A

S phase

  1. Cdk and Ddk (cyclin dependent kinases - inactive in G1) activate PreRCs
  2. Phosphorylation of several proteins leads ro DNA melting and protein recruitment.
  3. Phosphorylation by S-phase cyclin kinases is necessary for replication fork assembly and confines the initiation of replication to S phase.
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11
Q

Cdk activity low

G1 phase

A

Pre RC formation allowed

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12
Q

Cdk activity high

S phase

A

Existing PreRC activation

CDK phosphorylates helicase loaders, preventing them to bind to ORC

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13
Q

When are histones synthesized

A

only during S phase and are added as replication proceeds

Some histone parts are “inherited” some are new

The spacing of histones every 200nt might be the reason for shorter okazaki fragments in eukaryotes and the slower speed of replication

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14
Q

The “end replication problem” (in eukaryotes)

A

both ends will be affected!

Results in incompletely replicated DNA due to okazaki fragments.

When completing DNA replication, the lagging strand will have okazki fragments, and the RNA primer fragments have to be removed from the strand by polymerase alpha. This leads to a shorter strand in the end of the newly synthesized DNA.

https://www.youtube.com/watch?v=wf6QiIlGxSg

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15
Q

Telomeres are the ends of the chromosomes

A
  • Protect ends
  • Maintain length
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16
Q

Telomere sequence identified as

A

Simple tandem repeats: TTGGGG

Tetrahymena Thermophila: Single celled pond animal with 40,000 short, linear chromosomes

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17
Q

Telomere repeats in humans

A

TTAGG

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18
Q

Telomere shortening leads to

A

cell death or cell senescence

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19
Q

Telomerase reverse transcriptase (TERT)

A

carry a tighlty bound, noncoding telomerase RNA (TR)

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20
Q

Telomerase:

A

TERT-TR holoenzyme (10ptn subunits + RNA of 451 nucleotides)

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21
Q

what type of protein is telomerase

A

ribonucleoprotein

  • RNA component from 150-1300 nt long. Serves as a template (3’AAUCCCAAU…5’)
  • Protein component has catalytic activities
    1. DNA polymerase - adds dNTPs to 3’ end of a linear DNA
    2. Reverse transcriptase, that carries its own RNA template
    3. DNA/RNA helicase activity
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22
Q

DNA polymerase adds

A

dNTPs to 3’end of a linear DNA

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23
Q

Reverse transcriptase

A

carries its own RNA template

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24
Q

DNA/RNA

A

helicase activity

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25
Q

Telomerase solve the “end replication problem” in eukaryotes

A
  • telomerase extends the 3’ end of the TEMPLATE strand, by adding dNTPs
  • Telomerase is a DNA pol and a reverse transcriptase
  • Telomerse is very different from other DNA pols: own template, and it synthesizes ssDNA
  • After adding a nt repeat, telomerase seperates the RNA-DNA hybrid and repositions on the telomere for extension of the next repeat
  • The telomerase-extended 3’ ssDNA terminus is converted to duplex DNA by the same priming and polymerization machinery used in chromosomes replication.
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26
Q

Telomerase characteristics

A
  • is a DNA polymerase and a reverse transcriptase
  • is very different from other DNA polymerases: own template and it synthesizes ssDNA
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27
Q

Telomeres replinished by

A

telomerase

Active: stem cells, germ cells
detectable: many normal adult cell types (quantifiable activity)

In humans ^

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28
Q

Telomeres shorten

A

during ageing of human fibroblasts

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29
Q

Long telomeres (before telomere shortening)

A
  • Maintenance of genome stability
  • Robust proliferation capacity

Telomerase activity
Low oxidative stress
Antioxidant vitamin intake
Psyvhological wellbeing
Physical Activity

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30
Q

Short telomeres (after telomere shortenig)

A
  • Loss of productive structures
  • DNA damage responses
  • Limited replication potential
  • Cellular senescence

Ageing
Stress
Obesity
Smoking
Viral infections
Chronic inflammation
Hormone imbalance
Acohol consumption
Air pollution

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31
Q

Abnormally short telomeres (associated with disease)

A

Premature aging syndromes
- diabetes
- osteoporosis
- Impaired function of the immune system
- cardivascular disease

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32
Q

Clue to longetivity of telomeres
“Fountain of youth”?

A

Telomeres are caplike features at the ends of chromosomes that help protect them when cells divide

Over time, due to ongoing cell division, telomeres become shorter. Telomere length appears to be an indication of age and the general health of an individual

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33
Q

Activation of telomerase

A

Increased incidence of tumors

  • maintenance of telomeres are essential to all cell growth
  • Inhibiting telomerase would theoretically kill cancer cells (they are immortal)
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34
Q

Telomeres are protected and regulated by proteins: Telomere binding proteins (in mammals, Shelterin)

A

Sheltrin
- regulate telomerase activity (prevent telomeres from growing abnormally long) and protect chromosomes from joining and exonucleases

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35
Q

Telomere Loop (t-loop)

(protection of telomeres)

A
  • T-loop buries the 3’ terminus of the telomere which further regulates telomere length.
  • 3’ end not accessible
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36
Q

Telomeres are requited for

A

chromosomes protection

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37
Q

Telomerase is essential for

A

telomere maintenance

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38
Q

telomere shortening leads to

A

cell death after many cell divisions

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39
Q

short telomeres limit

A

the growth of cancer cells

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40
Q

short telomeres limit tissue renewal and

A

contribute to age-related degenerative disease

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41
Q

Mutations are …

A

changes in DNA sequence that is propegated through cellular generations

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42
Q

When mutations occur in germ line cells

A

the changes are inheritable

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43
Q

Some frequency of mutation

A

is necessary to produce the variability on which natural selection acts to drive evolution

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44
Q

Mutations can occur through many different mechanisms, but

A

all originate as an alternation in DNA

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45
Q

Only after the alteration is converted through replication into an incorrect base pair…

A

such as AT where, GC should be, does it become a stable inheritable mutation.

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46
Q

The vast majority of damaged nucleotides that occur in a mammalian cell every day..

A

are repaired by DNA repair enzymes

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47
Q

Point mutations

A

single base pair substitutions

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48
Q

Mutations of one or few base pairs usually result from

A

errors in replication or damaged nucleotides

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49
Q

transitions are nearly

A

10 times more frequent than transversions

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50
Q

Transition examples

A

Purine to purine (A to G, or T to C)

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51
Q

transversion examples

A

purine to pyrimidine (A and G turn into C and T)

Pyrimidine to purine (C and T turn into A and G)

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52
Q

point mutations have an effect on

A

the protein sequence

  • A point mutation in the protein coding region of a gene can result in an altered protein with partial or complete loss of function
  • Point mutations are known to cause a wide variety of human diseases
  • Point mutations in a protein-coding region can be classified by their effect on the protein sequence: Silent, missense and nonsense mutations
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53
Q

Silent mutation

A

TTT - AAA

lysine stays lysine

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54
Q

Nonsense mutaitons

A

creation of a stop codon.

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55
Q

Missense mutaiton

A

formation of a new amino acid.

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56
Q

DNA top strand

A

= coding = sense = non-template

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57
Q

DNA Bottom Strands

A

= template strand = antisense = noncoding.

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58
Q

RNA has same sequence as DNA

A

top strand; is complementary to DNA bottom strand

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59
Q

The genetic code

A

The DNA sequence encoding a protein is read in triplets or codons

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60
Q

61 of 64 codons are

A

sense codons for amino acids

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61
Q

3 of 64 codons are

A

nonsense or termination / stop codons.

62
Q

AUG codon significance

A

served as a start codon

63
Q

the genetic code is degenerate

A

a single AA can be encoded by more than one codon (20 AA)

64
Q

Stop codons examples

A

UGA
UAG
UAA

65
Q

Nonoverlapping

A

triplets are ready from a fixed point

66
Q

open reading frame (ORF)

A

a run of sense codons (more than 25) before a stop codon is encountered

67
Q

Silent mutations

A
  • mutations in non-coding and or/non-regulatory regions
  • Mutations in coding region - because of code degeneracy may result in the incorporation of the same amino acid

Ecample: A change of TTC (mRNA: AAG) to TTT (mRNA: AAA) is silent because both are codons for Lysine (they are synonymous)

68
Q

Missense mutation

A

any mutation within coding region leading to a change of one amino acid for another

  • Severity will depend on the nature and the “location” of the change.
69
Q

sickle cell anemia caused by

A

missense mutation in the gene that encodes for the beta subunit of the protein hemoglobin

Beta 6th position (Glutamic acid - Valine)

70
Q

Normal hemoglobin

A

Function: molecules do not associate with one another; each carries oxygen

71
Q

Sickle cell hemoglobin

A

Function: molecules interact with one another to crystallize into a fiber; capactiy to carry oxygen is greatly reduced.

72
Q

Nonsense muations

A
  • Changes in nucleotides, leading to stop codon.
  • Stop codon terminates translation and generates a truncated protein, without a complete AA sequence.
  • The severity of a nonsense mutation will depend on the location
73
Q

Point mutations : a 2 step process

A
  1. DNA polymerase incorporates an incorrect nucleotide
  2. If the mismatch is not required, it becomes a mutation in a second step during replication
74
Q

Insertion and deletions are

A

indels

75
Q

Insertion

A

occurs when one or more base pairs are added to the wild type sequence
- may have no effect if not in genes or regulatory sequences
- leads to usually a truncated protein

76
Q

deletion

A

due to loss of one or more base pairs
- may have no effect if not in genes or regulatory sequences
- leads to usually a truncated protein

77
Q

indel mutation

A

of only one or two base pairs in the coding dequence of a protein throws off the reading frame after the mutation, resulting in frameshift mutation.

78
Q

Indels of 3 or multiple of 3 nucleotides

A
  • preserve the reading frame
  • most common: insertion of 3 nucleotides (template slippage by DNA pol during replication)
79
Q

indels are caused by

A

aberrant recombination or by templare slippage by the DNA polymerse during replication

80
Q

Insertion of triplet sequences and human disease

A
  • Triplet expansion diseases
  • More than half of the triplet expansion diseases: expansion of the CAG codon for glutamine (Q) - polygrutamine (PolyQ) diseases
81
Q

DNA alterations that leads to mutations

A
  • Spontanous hydrolysis (water)
  • Oxidative damage (reactive oxygen species - ROS)
  • Alkylation (alkylating agents)
  • Radiation (UV light, X rays , etc)
82
Q

Spontaneous DNA damage by hydrolysis

A

Deamination (C,G or A) or loss of bases by hydrolysis

83
Q

Deamination

A

removal of an amino group - changes “identity” of bases and their pairing properties

Cytosine to uracil
5-Methylcytosine to thymine

Approx 5% Cs in higher eukaryotes are 5-mC

84
Q

Deamination of G or A

A

much less frequent (approx 100x) and produces “abnormal bases”

Guanine becomes Xanthine
Adenine becomes Hypoxanthine

85
Q

Loss of bases by hydrolysis

A

depurination much more frequent than depyrimidaiton

1 in 10^5 purines (per 10,000 mammalian cell) are lost from DNA every 24 hrs.

86
Q

Oxidative damage and alkylating agents can create

A

point mutations and strand breaks

87
Q

Deamination by nitrous acid

A

Sodium nitrate (a common food preservative) as well as nitrosamines are converted to nitrous acid in the stomach.. nitrous acid is a potent mutagen.

88
Q

Oxidative DNA damage

A
  • possibly the most important source of mutagenic alterations in DNA
  • ROS: hydrogen peroxide (H2O2), hydroxyl radicals (OH-), superoxide radicals (O2-), arise during irradation or as byproducts of aerobic metabolism
  • Oxidative damage includes modification of bases, sugar, removal of bases and strand breaks.
89
Q

8-oxoG

A

Guanine -> 8-Oxoguanine

90
Q

8oxoG is very mutagenic because it can pair with A leading to _ if not repaired prior to replication

A

Transversion

91
Q

Most common mutation found in human cancers

A

G:C to T:A transversion

92
Q

Damage by alkylation

addition of an alkyl group, usually to bases

A

Alkyl groups
- methyl
- ethyl
- propyl
- isopropyl

93
Q

O^6-MethylG is very mutagenic becuase it tends to pair with T instead of C leading to _ ?

A

transition

94
Q

Benzo[a] pyrene (intercalating agent, carcinogen)

A

smoke of brunign cigarettes, wood, and coal.

In the liver, it becomes a reactive epoxide that can react with bases.

95
Q

Nitrogen mustard gas (damage by alkylation)

A

Cross linking agents that react with adjacent G residues preventing replication and transcription

96
Q

DNA damaging agents are used in Cancer chemotherapy

A

DNA reactive agents used in chemotherapy for cancer kill cells (cytotoxic) by creating broken chromosomes or stalled replication forks, either of which leads to cell death during cell division.

97
Q

Ames test
What does it test for?

A

This test is used to determine mutagenic potential of chemicals in animals

Identifies DNA damaging chemicals

98
Q

The Ames test for mutagens and carcinogens

A
  • Use histidine auxotrophic (his) Salmonella typhimurium - mutation in biosynthetic pathway for histidine (requires histidine in the growth medium)
  • look for His+ revertants
99
Q

reversion mutation

A

can synthesize his and grow in his-free medium)

Chemical is a mutagen!

100
Q

Most known human carcinogens result in

A

increased mutation in the Ames Test

101
Q

compounds identified as mutagens in an ames test require…

A

further testing to determine whether they are likely to be human carcinogens.

102
Q

Ionizing radiation

A

UV light (in sunlight), cosmic rays, X-rays

103
Q

UV and other ionizing radiation

A

about 10% of all DNA damage caused by environmental agents

UV can cause photochemical fusion of adjacent pyrimidines (pyrimidine dimers - covalent cross links)

104
Q

Xrays and Gamma rays (higher energy)

A

Single or doubled strand DNA breaks

105
Q

Skin cancer major risk

A

A major risk is prolonged exposure to ultraviolet (UV) radiation.

  • Just one indoor tanning session can increase your melanoma risk
  • ## Every time you burn or tan, you increase damage of DNA. the more you dmage your DNA, the greater your risk of getting skin cancer.
106
Q

Deadliest form of skin cancer

A

Melanoma

107
Q

Tanning beds

A
  • 97% of women diagnosed with mleanoma before the age 30 have engaged in indoor tanning
  • Just one indoor tanning session before the age of 35 increases a person’s risk of melanoma by 75%
  • Tanning - indoors or with the sun, makes your skin age more quickly
108
Q

Squamous cell carcinoma (SCC)

A
  • one tanning session causes a 67% increased risk of developing SSC
109
Q

Basal cell carcinoma (BCC)

A

one tanning session causes a 29% increased risk of developing BCC

110
Q

Summary: DNA mutations

A
  • Hydrolysis can deaminate nucleotide bases, altering their ability to base pair and leading to mismatch during replication
  • hydrolysis can also sever the glycosyl bond between the pentose and the base, leaving an abasic site
  • Nitrous acid, the metabolic product of food preservative, can induce the deamination of A or C residues, resulting in a transition mutation
  • Oxidative damage is caused by reactive oxygen species that react with nucleotides at many different positions in the molecule. Oxidation can affect base pairing or cause DNA strand breaks
  • Alkylating agents attack DNA and add bulky chemical groups to the base or the ohosphodiester backbone. Alkylation can alter the base pairing of the nucleotide
  • DNA damaging agents can lead to muations at low concentrations and can kill the cell ay high concentrations
111
Q

The ames test determines whether a compound is

A

mutagenic in bacteria, thus identifying the compound as a potential carcinogen

112
Q

UV light from the sun

A

can form pyrimidine dimers, that stall DNA polymerase during replication

113
Q

Mismatch repair (MMR)

A

involves a removal of several to many nt’s from new strand

114
Q
  1. Photoreactivation
A

photorepair of cyclobutane pyrimidine dimers

115
Q

DNA photolyase

A

uses the energy derived from absorbed visible light to reverse damage of UV light

116
Q

Photolyases: present in all almost all cells

A

Bacterial, archael and eukaryotic. Yet, for some reason are not present in the cells of placental mammals (including humans).

117
Q

chromophore

A

light absorbing group

118
Q

Direct reversal of DNA damage (Direct repair)

A
  1. Photoreactivation
  2. Removal of alkyl groups
119
Q

removal of alkyl groups

A

repair oxidized nucleotides (O^6-methylguanine). Requires specific enzymes

120
Q

O^6 methylguanine-DNA methyltransferase

A

catalyzes transfer of methyl grpup of O^6 methyl guanine to one of its own Cys residues

121
Q

O^6 methylG is very mutagenic because it tends to pair with T instead of C, leading to_?

A
122
Q

Base Excision Repair (BER)

A

Functions at the level of single damaged nucleotide and it is involved in several types of repair mechanisms.

  1. Removal of single “damaged” base (alkylation, oxidation, or deamination); most U’s are removed by BER
  2. Removal of abasic sugar (recognition and repair of AP sites)
  3. This is a main mechanism for repairing of single strand breaks that don’t have the proper ends for ligase, “clean up” for ligase
123
Q

DNA Glycosylase

A

recognition of the damaged base

124
Q

Glycosylases scan DNA and “flip”

A

damaged base out of the helix… and remove it if it fits in the catalytic site

125
Q

DNA glycolysas - two main types:

A
  1. highly specific to a particular damaged base
  2. Recognizes oxidative damage (diverse substrate spectrum).
126
Q

Nucleotide Excision Repair (NER)

A

Targets large, bulky lesions and removes DNA on either side of them.

  • Protein complexes recognize a variety of base damages resulting distortions to DNA structure. In contrast to BER, NER does not require specific recognition of a damaged nucleotide.
  • NER enzymes cleave damaged DNA strand on both sides of the “lesion” (removing more than the damage itself)
  • Specialized helicase “releases” cut fragament
  • DNA polymerase fills in the single gap using undamaged strand as a template
  • Ligase closes the nick.
  • Predominant repair pathway for removing pyrimidine dimers, 6-4 photoproducts, and several bulky base adducts, including benzo[a] pyrene-guanine.
127
Q

NER in E.Coli

A

Involves primarily four proteins (UvrA, UvrB, UvrC, UvrD)
- UvrA2 UvB complex scans for NDA distortionsm (damage)
- UvrA leaves
- UvrB melts short stretch of DNA
- UvrC nicks both sides of distortion. (about 12-13 bases) (exinuclease)
- UvrD (helicase) releases the oligonucleotide
- DNA Pol. I fills in and ligase closes the gap.

128
Q

NER in eukaryotes

A

Main factors discovered through reasearch on XP patients (Xeroderma pigementosum)
- individuals extremely sensitive to singlight, thousands of times more likelu to develop skincancer
- Most patient develop neurological abnormalities
- Mutations in at least seven genes (XPA-XPG) result in XP (defective NER)

129
Q

NER is the sole repair

A

pathway for pyrimidine dimers in humans

130
Q

TCR

A

Transcription-coupled repair
Specifically targets repair to actively transcribed DNA

131
Q

DSBs

A

(double strand breaks) can be repaired by homologous recombination (error “free”) - typical route

132
Q

Phases of the cell cycle when no sister chromatids are present –>

A

NHEJ - (non homologous end joining)
is a repair system for DSBs (double strand breaks) - usually leads to loss of DNA (produce mutations)

133
Q

UvrA

A

recognzies lesion

134
Q

UvrB

A

Unwinds DNA

135
Q

UvrC

A

Exinuclease

136
Q

UvrD

A

Helicase

137
Q

Pol I

A

fills in gap

138
Q

DNA ligase

A

seals DNA

139
Q

NHEJ

A

Non homologous end joining

All eukaryotes; detected in some bacteria

140
Q

Translesion DNA synthesis

A

lesion at a replication fork after the DNA strands have been unwound

141
Q

Damaged DNA is encounteres by the fork

A

Specialized TLS DNA polymerases are employed

142
Q

TLS DNA Pol:

A
  • error prone: Usually lacks proofreading activty (low fidelity)
  • Extends DNA strand across bulky template lesion (often results in a mutation)
143
Q

TLS polymerases in humans

A

10

144
Q

mismatch repair system corrects

A

nucleotide residues misincorporated during replication

145
Q

some types of lesions are repaired directly, such as

A

photoreversal of pyrimidinse dimers by photolyase

146
Q

The base excision repair pathway corrects relatively small,

A

single base lesions and uses different DNA glycosylases to recognize particular lesions

147
Q

nucleotide excision repair system repairs

A

bulky lesions by using exinuclease that makes strand incisions on either side of the lesion

148
Q

Transcription coupled repair

A

adapts the nucleotide excision repair system to lesions identified by a stalled RNA polymerase

149
Q

Double stranded DNA breaks result in

A

fragmented chromosomes and are usually repaired by homologous recombination, a highly fidelity process

150
Q

Double strand breaks can also be processed by

A

error-prone nonhomologous end joining

151
Q

Cells contain multiple

A

specialized DNA polymerases that extend DNA across lesions, but translesion synthesis is usually error-prone process that results in mutation

Molecular Genetics (9 decks)

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