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MICR2208.2 > L24: Mutation And DNA Repair In Bacteria > Flashcards

L24: Mutation And DNA Repair In Bacteria Flashcards

1
Q

Gene

A

The nucleic acid sequence that codes for polypeptide, tRNA or rRNA

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2
Q

Genotype

A

Collection of genes an organism has, or its genetic composition

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3
Q

Phenotype

A

Observable characteristics of an organism, or expression of genes

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4
Q

Mutation

A

Permanent, heritable change to base sequence of DNA

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5
Q

Wild type

A

Organism as it was first isolated from nature. Considered to be normal type

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6
Q

Mutant

A

Organism that differs from wild-type as result of mutation

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7
Q

Mutation of DNA

A

Rare

Main cause: errors in DNA replication (incorrect base inserted into daughter DNA strand)

  • > detectable mutation rate at ~1 in 10^7 to 10^11 per bacterial cell for any particular gene
  • > sensitive detection systems needed
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8
Q

DNA damaged by mutagens

A

DNA modifying agents: e.g. add alkyl groups to bases, change base pairing, such as ethylmethane sulphonate (EMS) which adds ethyl groups

Intercalating agents: planar compounds which insert into DNA helix and distort backbone (e.g. acridine orange, ethidium bromide)

Physical agents:
UV induced thymine dimers- DNA absorbs UV at 260nm, forms intra-strand pyrimidine dimers, mainly T-T, distortion of double helix ->
prevent replication
Oxygen radicals- cause single and ds breaks -> prevents replication (e.g gamma and x-rays)

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9
Q

Point mutations

A

Base substitution: transition (purine -> purine, pyrimidine -> pyrimidine) and transversion (pyrimidine to purine)

Base addition or deletion

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10
Q

Greater than one base change mutation

A
  1. Addition of deletion of multiple bases
  2. Inversion of segment of DNA
  3. Duplication of segment of DNA
  4. Translocation
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11
Q

Effects of DNA mutation on encoded protein

A

Synonymous (silent) mutation

Missense mutation (conservative, non-conservative)

Nonsense mutation

Frameshift mutation

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12
Q

Silent mutation

A

No effect on mutation

Genetic code is redundant. Codes encode same AA

If mutation occurred to swap codons around -> no effect on protein

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13
Q

Missense mutation

A

One AA in protein is replaced by another

Conservative: replacement with AA of similar biochemical profile -> no loss in protein function

Non-conservative: replacement with AA with different biochemical profile -> complete loss of function or partial loss of function (leaky mutant)

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14
Q

Nonsense mutation

A

Gives rise to stop codon

TAG, TGA, TAA- stop or nonsense codons which do not encode for an AA, but signal stop translation

Possible effects: limited effect on protein if close to end of open reading frame or cause complete loss of function as premature termination of polypeptide chains -> truncated protein

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15
Q

Frameshift mutation

A

Caused by nucleotide deletion or insertion of one or more bases -> change in codon reading frame -> change in AA incorporated into protein

-> loss of function but depends on location within gene

Indels not in no. divisible by 3 -> frameshift

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16
Q

Revertant

A

Strain in which 2nd mutation bas restored phenotype altered by 1st mutation

  1. True reversion (back mutation): original sequence is restored (ATG -> ATC -> ATG). Point mutations revert, large deletions do not
  2. Suppression (2nd site mutation): a change at a different site in genome that phenotypically corrects the 1st mutation which is still present
    a) intragenic suppression: 2nd mutation is same gene as 1st mutation
    b) extragenic (intergenic) suppression: 2nd mutation is a different gene from 1st mutation. Example: mutation in anti-codon of tRNA (2nd mutation) may allow tRNA to recognise nonsense stop codon (1st mutation) and allow protein translation. Mutation -> poor growth
17
Q

Direct detection mutants

A

Screening (visual observation or other phenotype)

Disadvantages of screening: very labour-intensive; not all mutations can be visually detected

18
Q

Indirect detection of mutants: replica plating

A

Auxotroph has defect in biosynthetic pathway (prototroph is wild type)

Unable to synthesise an essential nutrient

Unable to grow unless supplied with that nutrient

19
Q

Indirect detection of mutants: selection

A

Use incubation conditions under which mutant will grow but wild-type will not

Examples pf selectable mutants: antibiotic-resistant mutant, bacteriophage (virus)-resistant, temp-resistant, phototrophic mutant

20
Q

Direct DNA repair mechanism

A

Restoration to original undamaged state

Photoreavtivation: photolyase enzyme absorbs energy from 350-500nm light, cleaves dimers back to monomers

Nucleotide excision (short patch) repair

Mismatch repair

21
Q

Indirect repair

A

Damage bypass system using DNA replication

Recombination repair: post-replication repair

SOS repair: bypass repair or error-prone repair

22
Q

Nucleotide excision repair

A

Products of uvrA, uvrB, uvrC genes form UvrABC exinuclease/UvrABC endonuclease

UvrAB complex migrates up and down DNA until it hits a distortion e.g thymine dimer

UvrA released, UvrC binds and cuts DNA ~4 nt 3’ and 7’nt 5’ of dimer

UvrD helicase helps to remove damaged fragment and UvrBC complex

DNA pol I copies intact strand to fill in gap 3’-5’ using 3’OH primer. Continues repair synthesis for few nt downstream, degrading DNA via its exonuclease activity and simultaneously replacing it

Sealed by DNA ligase

Called ‘short base repair’ as about 13nt replaced

23
Q

Mismatch repair

A

During DNA rep, DNA pol III has 3’-5’ exonuclease activity (proof-reading/editing function) -> excises incorrectly base-paired nt at 3’OH end in replicating DNA

Incorrect bases not at 3’end are recognised -> excised by complex containing MutS and MutL (mismatch recognition/excision enzymes) and MutH (strand recognition protein binds methylated DNA)

Complex binds to methylated GATC sequence

24
Q

Recombinational repair

A

DNA replication stalls at thymine dimer (DNA pol III adds A, removes A via its 3’-5’ exonuclease editing or proof-reading activity, adds A, removes it etc.)

DNA synthesis reinitiated beyond dimer but gap is lethal to cell

RecA protein binds to ss gap, initiates recombination which fills gap, but leaves gap in parental DNA

Gap filled by DNA pol copying undamaged strand, and DNA ligase

Dimer remains but DNA synthesis can continue, cell survives, has chance to remove dimer vis nucleotide excision repair mechanism

25
Q

Holliday junctions

A

Branch migration: holliday junctions move up and down DNA by breakage and rejoining of HB between bases. Can occur spontaneously but is sped up by ATP-hydrolysing RuvAB proteins

How do the 2 DNA molecules separate?

If linear DNA, branch migrates off end

If circular DNA, Holliday structure is resolved by RuvC protein cutting them apart

MICR2208.2 (16 decks)

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