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GENE221 > Lecture 4 > Flashcards

Lecture 4 Flashcards

1
Q

What is a mutagen

A

an agent capable of increasing the frequency of mutaion

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2
Q

What kind of mutaions do mutagens mainly induce?

A
  • most increase the frequency of substitution mutations
  • some result in indels
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3
Q

3 examples of mutagens

A
  • EMS
  • aminopurine
  • UV light
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4
Q
A
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5
Q

Different mutagens have different ____ - they can use different ____ in the ____

A

Effects
Mutation
DNA

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6
Q

How do chemical mutagens work?

A
  • by modifying base - pairing properties
  • DNA polymerase then incorporates wrong bases during DNA replication
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7
Q

3 key mutagens

A
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8
Q

What is EMS and what mutaion does it cause

A
  • EMS is an alkylating agent
  • causes GC —-> AT mutations

(Gaunine changes chemical properties which makes binding to thymine more favourable)

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9
Q

EMS pre mutaion lesion

A
  • ethyl on guanine
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10
Q

EMS mutaion diagram

A
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11
Q

2 amino purring mutaion - a base analogue - what happens when adenine changes to 2-AP?

A
  • most often pairs with thymine but can also base - pair with cytosine
  • if this happens during replication, will lead to an A-T basepair being changed to A-C and subsequently G-C
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12
Q

What is aflatoxin produced by?

A

Fungi

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13
Q

What does aflatoxin do?

A
  • chemically reacts with guanine (G) bases in DNA (interferes with back bone)
  • causes GC —> TA mutations
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14
Q

Reaction of aflatoxin B with DNA generates _________ _____ this can lead to _______

A

Apurinic sites
Mutation

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15
Q

What are apurinic sites?

A

Apurinic sits are the result of depurination - a purine base (adenine or guanine) is lost from the DNA

  • Apurinic site thus is a sit without a purine
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16
Q

Why do apurinic sites cause mutations?

A
  • during DNA replication, there is a blank where the purine should be
  • a base (often an adenine) may be inserted opposite the blank
  • this can change the sequence of base-pairing
17
Q

Can DNA polymerases synthesise past “damaged” DNA (lesions) such as apurinic sites? What is used instead?

A

No
Instead special “bypass” DNA polymerases do this (translesion DNA synthesis)

18
Q

Are bypass DNA polymerases as accurate as normal DNA polymerase? What does this result in?

A

No, they are much more likely to incorporate the wrong base even when the DNA is not damages leading to mutaions

19
Q

Process of trans-lesion DNA synthesis

A

It is initiated by stalled DNA polymerase (stalled cos there is a lesion and it doesn’t know what to do), which triggers recruitment of a TLS polymerase that synthesises past the lesion

Once extension passes the lesion, the TLS polymerase is replaced by the replicative DNA polymerase

20
Q

3 main effects of mutagens causing mutaions and what they all require

A
  • chemical mutagens alter bases in the DNA and affect base-pairing (like EMS)
  • some mutagens “mimic” normal bases and become incorporated into the DNA, then later pair with the “wrong” bases (like 2-AP)
  • other mutagens result in the absence of a “pairable” base during DNA synthesis (like aflatoxin)

ALL mechanisms require DNA replication to become mutations!!!! <—- take home message!

21
Q

What is a pre-mutagenic lesion?

A

A change to the DNA that may lead to a mutation

22
Q

Where does DNA repair systems take place? And why?

A
  • at least one round of DNA replication is needed to get from a pre-mutagenic lesion to a mutation
  • DNA repair takes place at the pre-mutagenic lesion (because ones the mutation is “established”, it is too late)
  • DNA repair systems repair “damages” DNA BEFORE it is replicated
23
Q

How do you repair EMS damage?

A
  • repair the proteins using alkyltransferases
  • the (alkyl) ethyl group is transferred from the base in the DNA to the protein
  • thus it can still pair with its correct pair
24
Q

Process of Repair of Apurinic sites

A
  • an enzyme (AP endonuclease) recognises an apurinic site and cuts the strand of DNA that contains it
  • the defective DNA and some adjacent DNA is then removed by a set of enzymes (excision exonucleases
  • the cap is filled my DNA synthesis
  • an example of excision repair
25
Q

How radiation (e.g ultraviolet light) causes mutations

A
  • adjacent thymidine (T) bases in the DNA can become covalently cross-linked - photodimers
  • these fail to base-pair properly during DNA replication
  • Translesion DNA polymerases can replicate past these but may incorporate the wrong base
26
Q

How to repair photodimers

A
  1. Nucleotide excision repair
    - similar to repair apurinic sites
  2. Photolyase enzyme
    - this uses energy from white light to convert photodimers back to pyrimidines (photorepair)
27
Q

Do the molecular mechanisms (repair systems) in bacteria also apply to eukaryotes ?

A
  • DNA sequencing shows that the molecular nature of mutations in humans is the same as in bacteria
  • higher eukaryotes have repair systems that are equivalent to those that have been identified in bacteria
  • defects in DNA repair have been associated with neurodegeneratice disorders and xeroderma pigmentosum - exceptional sensitivity to sunlight
28
Q

How some e.coli bacteria can use mutagens as weapons

A
  • some coli bacteria that can live in the human gut secrete a compound called Colin actin
  • this can react with DNA in human cells and lead to mutations
  • related to colorectal cancer
29
Q

Take home messages

A
30
Q

Researcher that used experimental system bacteriophage T4

A

Seymour benzer

31
Q

What did Seymour benzer do?

A

Experimental system bacteriophage T4
- dont mix up with T1 from earlier lecture

32
Q

What is a bacteriophage

A

Viruses that infect bacteria

33
Q

Why did benzer use bacteriophage ?

A
  • easily and rapidly grown
  • genetically amongst the simplest organisms
  • they have similar genetic mechanisms to the host cells
  • can analyse many billions very easily
34
Q

What are bacteriophage plaques ?

A

“Holes” in a lawn of bacteria where bacteria have been killed by the phage

35
Q

rII gene mutant phage vs wild-type bacteriophage T4

A
  • Wild-type T4 can infect two different kinds of E.coli bacteria, strains K and B
  • rII mutant phage forms large plaques on E.coli strain B but CONNOT form plaques on E.coli strain K
36
Q

Definition of complementaion

A

Production of wild-type phenotype when two mutant haploid genomes bearing different recessive mutations are present in the same cell

37
Q

What did benzer do to show compliemntaiton

A
  • infected pairs of rII mutants into E.coli K12
38
Q

Benzer complementaiton system diagram

A

GENE221 (23 decks)

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