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LF104 - MCO #2 > Mutagenesis > Flashcards

Mutagenesis Flashcards

1
Q

Why do we study mutants?

A
  • Aid in developing biochem + cellular knowledge.
  • Useful in biotech
  • Bacterial mutations = same mechanisms in humans for e.g. cancer.
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2
Q

How do bacteria repair/fight against mutations?

A
  • Enzymes repair DNA
  • Melanin + other pigments = protect from radiation.
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3
Q

How can bacterial DNA be mutated?

A
  • DNA polymerases make mistakes when polymerising DNA
  • Causes spontaneous mutations.
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4
Q

What are 3 examples of spontaneous mutations?

A
  1. Replication errors
  2. Tautomers
  3. Base pair slipping
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5
Q

What are replication errors?

A

Wrong base substitution by DNA Pol

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6
Q

What are tautomeric mutations?

A

DNA base pairs w spontaneous change in structure (become tautomers) = mismatched in DNA replication.

e.g. Adenine normally w Thymine instead tautomeric A = pair w Guanine.

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7
Q

What is base pair slipping?

A

Repeat nucleotides cause frameshift mutations - no longer in groups of 3 by adding/removing nucleotides.

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8
Q

How can increase mutation rate?

A

Mutagens: - chemical/physical agent that damages DNA

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9
Q

How do intercalating agents affect mutation rate?

A

Intercalating => inserting substance into DNA + binding btwn BPs.
- Distort double helix + cause frameshift mutations

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10
Q

What are point mutations?

A

One BP changes e.g. substitution CATG -> AATG

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11
Q

Is inserting/removing a BP a point mutation?

A

Some say = “indel” instead.

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12
Q

Different substitutions in DNA

A
  1. Transitions
  2. Transversions
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13
Q

What is a transition?

A

Point mutation - either subs 2 ring purines (A <-> G) or 1 ring pyrimidines (C <-> T).

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14
Q

What is a transversion?

A

Point mutation - DNA changing 2 ring purine (A/G) for 1 ring pyrimidine (C/T)

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15
Q

How does mismatched base pairs occur?

A
  • Replication errors
  • Tautamerisation
  • Damage e.g. deamination
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16
Q

Example of deamination causing mismatching:

A

e.g. deamination of adenine -> hypoxanthine.

1st daughter cell may get repaired via DNA pol
2nd daughter cell = carries mutation:
- H acc base pairs w C not T so C inserted instead.
- This means next division = one cell => C pairs w G so changes whole sequence, other cell => still mutated w H.

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17
Q

What is the result of mismatched base pairs?

A

Causes culture to be mixture of different genotypes (genes + genetics) and sometimes phenotypes (observable characteristics)

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18
Q

What are the consequences w point mutations?

A

Depends on where it occurs in bacterial genome

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19
Q

Do all point mutations lead to inherited characteristics?

A

No some mutations = lethal so not inherited.

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20
Q

What is consequence of point mutation on non-coding regions of bacterial DNA?

A
  • Maybe no consequences and isn’t significant
  • If part of regulation or promoter sequences = can be detrimental
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21
Q

What is consequence of point mutation on a promoter region of bacterial DNA?

A
  • Maybe insignificant.
  • May cause up/down regulation of transcription of certain proteins causing imbalances and potentially detrimental effects.
22
Q

What is consequence of point mutation on genes under promoter control in bacterial DNA?

A
  • Depends on mutation and where in coding region occurs.
  • Could affect sequence of DNA or regulator of translation
23
Q

How much DNA in bacteria + archaea is non-coding?

A

6-14%, much less than eukaryotes = more chance for mutation to affect protein coding sequence.

24
Q

What are types of mutations in protein coding?

A

Silent -> e.g. 3 genes to code for Arginine = swap one for other doesn’t affect anything.

Missense -> mutation changes whole amino acid coded for.

Nonsense -> mutation changes amino acid code into STOP codon, halting synthesis of protein in that location.

25
Q

Effect of silent mutation in coding sequence on protein

A

Silent -> Genotype change not phenotype.
i.e. overall no net change in protein.

26
Q

Effect of missense mutation in coding sequence on protein

A

Missense -> Genotype changes + potentially phenotype changed.
i.e. overall often no effect but potentially detrimental.

27
Q

Effect of nonsense + frameshift mutation in coding sequence on protein

A

Nonsense -> Genotype + phenotype changes.
i.e. usually detrimental but potentially tolerated near C-terminus (happens near end so most of code already there)

28
Q

What is a deletion mutation?

A

Removing chunk of genome, either base pairs or kilo-bases (removes whole genome areas)
Consequences:
- can cause frameshift mutation
- or affect coding/regulatory regions of gene.

29
Q

What is an inversion mutation?

A

Chunk of genome flips and is turned around.
Consequences:
- depends on where and what part affecting.
- No issues if gene turned round but issue if gene is cut in half (can’t work).

30
Q

What is a tandem repeat mutation?

A

Part of genome duplicates, potential to evolve proteins.
Consequences:
- Can cause overproduction of proteins if producing 2 copies.

31
Q

What are transposon mutations?

A

Transposons = “JUMPING GENES” nucleotide sequences insert themselves + move independently around DNA.
Consequences:
- Disruption of genes.

32
Q

How can mutations be reversed?

A
  • Point mutation restores original sequence.
33
Q

What is a suppressor mutation?

A

Second mutations that occurs causing restoration of original phenotype.

Intragenic suppression = suppression in same gene as original mutation

34
Q

What is intergenic suppression?

A

Second mutation suppressing another occurring in a different gene to the one in which first mutation occurs.

e.g. nonsense suppression

35
Q

Overview of translation

A

tRNA w anticodon binds to codon on mRNA and amino acids add in in right order.
tRNA w complementary sequence to codon of AA sequence they carry.

e.g. AAA for Lys -> anticodon = UUU

36
Q

How is nonsense suppression e.g. of intergenic suppression ?

A

STOP codon mutation added into mRNA => so tRNA anticodon is mutated to understand the STOP codon and instead inserts another AA into site enabling translation to continue to occur.

37
Q

What are amber mutations ?

A

UAG mutations that signal the end of translation.

38
Q

What is the mutant tRNA known as and functions?

A

supF = suppressor of amber (UAG) mutation via insertion of tyrosine at stop codon site.

39
Q

How do nonsense suppressors affect bacterial strains?

A

Normally unhealthy strains;
Cells translate past normal stop codons causing longer proteins w incorrect functions or folding.

40
Q

What does a triangle/delta symbol in genetics mean?

A

Deletion in gene or genetic information

41
Q

How can we select mutants in populations?

A

For selectable phenotypes e.g. drug resistance, plate w and without certain drugs in media.

For others: grow via replica plating under permissible and normal conditions.

42
Q

How to make a histidine auxotroph?

A
  1. Expose to mutagen
  2. Grow in complex medium.
  3. Transfer to minimal media w penicillin (only kills grown bacteria not auxotrophs which don’t grow)
  4. Plate on minimal media w histidine
  5. Check on replica plate is His auxotroph.
43
Q

What is phenotype lag?

A

The time taken for genetic change to manifest as a visible or measurable characteristic.

44
Q

How long does phenotype lag often take?

A

Often phenotypes not seen for multiple generation.

45
Q

Example of phenotype lag w T1 phage and EC?

A

Phage binds to protein encoded by tonB.
tonB mutation = stops protein synthesis, (>1000 copies already present).
2nd generation = 500 copies, 3rd = 250, 4th = 125 –> eventually cells w 0 copies leads to resistant EC to phage.

46
Q

What is cross feeding?

A

Different bacterial strains or species exchange metabolites or nutrients, to supporting each other’s growth or survival.
- Occurs when metabolites accumulate before block in metabolic pathway.

(only works if feedback regulation means metabolites can accumulate)

47
Q

What is the Ames test?

A

Widely used test that identifies mutagenic (therefore carcinogenic) chemicals.

48
Q

Assumption of the Ames test?

A

If chemical is mutagenic to bacteria it is also mutagenic to humans.

49
Q

Steps of Ames test

A
  1. Strains of S. typhimurium are picked that carry mutations to His biosynthesis, so cannot produce His.
  2. Plate these on minimal media, one w chemical other without.

Results:
If mutagenic, reversions should be abundant (mutagen induced DNA mutations)
If non-mutagenic reversions minimal.

50
Q

What are the limitations of the Ames test?

A

Chemical = maybe not mutagenic but metabolite could be and could alter chemical.

LF104 - MCO #2 (3 decks)

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