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Last Module Microbio Lec > Bacterial Genetics: Mutations > Flashcards

Bacterial Genetics: Mutations Flashcards

1
Q

Heritable changes in the base sequence of a genome

A

Mutations

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2
Q

Differentiate

Wild-Types vs Mutants

A

Wild-Type (WT)
* Contains normal gene, control

Mutant
* Possess changes in genome

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3
Q

Differentiate

genotype vs phenotype

How are they written?

A

Genotype
* Nucleotide sequence
* italics, 3 lowercase letters + 1 uppercase
* Ex. hisC gene

Phenotype
* Physical/physiological characteristics
* 1 capital letter + 2 lowercase + +/- superscript (says if microorganism expresses it or not)
* Ex. E. coli: His^+ if WT & has the gene, His^- if mutant & no gene (WT has the gene, mutant doesn’t)

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4
Q

Between His+ and His-
* Which is the WT and which is the mutant?
* Which one has the gene, and which one doesn’t have it?

A

His+: WT & has the gene
His-: mutant & no gene

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5
Q

Differentiate

Selectable Mutations vs Non-Selectable Mutations

What methods to they use to isolate mutants?

A

Selectable Mutations
* Can confer a clear advantage on mutant strain
* Allows them to survive better than WT
* Uses selection

Non-Selectable Mutations
* No advantage over other strains even if phenotype changes (Ex. change in pigmentation))
* Need to perform Screening instead

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6
Q

Explain

Selection

A
  1. Grow cells on media w/ antibiotic.
  2. Cells that grow are resistant to antibiotic
  3. WT is not resistant, but mutants are
  4. So mutant will grow
  5. Yay mutant is isolated
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7
Q

Explain

Screening

A
  • You can’t select the mutants, growth conditions will not kill WT
  • Grow both WT & mutant, then observe different characteristics
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8
Q

What does replica plating identify in a bacterial population?

A

Auxotrophic mutants

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9
Q

T/F

  1. Auxotrophs are mutants who do not need any other requirements for growth.
  2. Their WT counterpart are called heterotrophs.
A

F, F
1. Need additional requirements
1. phototrophs

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10
Q

How do we do replica plating?

A

Materials
* 2 agar plates: complete medium (w/ amino acid histidine), 1 w/o
* Master mix of prototroph & auxotroph colonies of E. coli

  1. Colony from master plate will be inoculated at exact spot in both media types
  2. Prototrphs grow normally in both
  3. BUT auxotrophs will not grow in medium w/o histidine
  4. Since you put them in the same places, you know that the missing slots are auxotrophs
  5. Isolate from those spaces
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11
Q

List

How do mutations occur?

2

A

Spontaneous mutations
* Naturally (ex. Errors in base pairing by DNA polymerases during DNA replication)

Induced mutations
* External agents (chemicals/radiation)
* Radiation can alter/damage DNA structure
* Chemicals can modify DNA (ex. nucleotide base analogs, alkylating agents, acridines)

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12
Q

List

Parts of Central Dogma

3

A
  1. DNA Replication
  2. mRNA Transcription
  3. Translation/Protein Synthesis
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13
Q

Explain

DNA Replication

A
  • DNA is replicated through DNA polymerases that use nucleotide base pairs of template strands
  • Adenine with Thymine, Cytosine with Guanine
  • DNA codes for proteins
  • Makes genes (DNA segments)
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14
Q

Explain

mRNA Transcription

A
  • DNA is copied through messenger RNA using RNA polymerases
  • Base pairs again, but A is with Uracil
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15
Q

Explain

Translation/Protein Synthesis

A
  • mRNA interacts w/ ribosomes to make proteins
  • Look for AUG (start codon)
  • Then it translates everything
  • Stops after UAA, UAG, or UGA
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16
Q

What are the start and stop codons?

A

Start: AUG
Stops: UAA, UAG, or UGA

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17
Q

What is the impact of a point mutation/base-pair substitution?

A
  • Change/substitution in 1 base pair
  • gene has a mutation → error in mRNA → faulty protein → diff phenotype
  • Pretty harmless tho
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18
Q

Why are Point Mutations / Base-Pair substitutions relatively harmless?

A
  • Since AA responds to several codons (1 acid = many codons), not all mutations will change something
  • Ex. if UUU mutates to UUC, phenylalanine pa rin naman yun
19
Q

List

Kinds of Point Mutations / Base-Pair Substitutions

5

A
  1. Silent
  2. Missense
  3. Nonsense
  4. Transition
  5. Transversion
20
Q

Differentiate

Silent Mutation vs Missense Mutation vs Nonsense Mutation

A
  1. Silent: Do not affect phenotype, 3rd base of codon
  2. Missense: leads to a diff AA, 1st/2nd bases, Causes sickle-cell anemia
  3. Nonsense: Stop codon is accidentally formed, Incomplete/truncated protein
21
Q

Differentiate

Transition Mutation vs Transversion Mutation

A
  1. Transition: same kinds replace (purine w purine, pyrimidine w pyrimidine) (A → G), (C → T)
  2. Transversion: Magkaiba (A → C or T → G)
22
Q

What disease is caused by Missense mutations?

A

sickle-cell anemia

23
Q

How are genes paired?

A

Adenine with Thymine (or Adenine & Uracil)
Cytosine with Guanine

24
Q

Describe

Frameshift mutations

A
  • The frame, shifts
  • If any base pair is inserted/deleted, the codons change, nag-iiba yung groups of 3
  • Most serious consequences
25
Q

Differentiate

Frameshift mutations w/ 1-2 base pairs vs Frameshift mutations w/ 3 base pairs

A

1 or 2 base pairs
* Changes reading frame of gene
* Changes primary sequence of polypeptide
* gain/loss of hundreds or thousands of base pairs
* Complete loss of gene function

3 base pairs
* No frameshift, but it adds/removes a codon
* 1 AA is deleted
* Not as bad as frameshift tho

26
Q

Differentiate

Same site/true revertant vs Second-site revertant

A

Same site/true
* 2nd mutation happens on same base pair

Second-site
* 2nd mutation on another pair
* Leads to suppressor mutation

27
Q

Define

suppressor mutation

Bonus: What can it do?

A

Makes up for effect of original mutation

Can
1. Restore enzyme function (2nd frameshift mutation near first, tas it restores original frame)
2. Restore function of original mutated gene
3. Produce enzyme to replace nonfunctional enzyme

28
Q

What is the typical mutation rate?

A

10^6 - 10^7 per thousand bases
* 1 round of replication
* Most are missense & silent mutations

29
Q

Identify

Chemical, physical, and biological agents that increase mutation rates of microorganisms

A

Mutagens

30
Q

List

Chemical Mutagens

3

A
  1. Nucleotide base analogs
  2. Alkylating agents
  3. Acridines/Intercalating agents
31
Q

Identify

  • Molecules w/ similar structure to purines & pyrimidines
  • Have faulty base-pairing properties
  • Can trigger replication errors

Ex. 5-bromouracil
* Analog of thymine
* Can pair normally w/ adenine
* But can also mispair w/ guanine

A

Nucleotide base analogs

32
Q
  • Chemicals
  • React w/ amino, carboxyl, & hydroxyl groups by substituting them w/ alkyl groups
  • Hyrdoxyl grps are in DNA
  • If alkyl group replaces hydroxyl → base-pair substitution or cross-links bet strands
  • Cross-links make the strands break
A

Alkylating agents

33
Q

What is the result of using Nucleotide base analogs vs using Alkylating agents?

A

Nucleotide base analogs: replication errors
Alkylating agents: cross-links that can break strands

34
Q

causes adjacent pyrimidines to dimerize (covalently bonded w/ each other)
Increases probability of DNA polymerase to misread DNA sequence & recruit wrong base pair

A

UV radiation (Nonionizing)

35
Q
  • Forms free radicals
  • can damage macromolecules in the cell (like DNA)
  • Leads to breaks → rearrangement/large deletions
A

Ionizing radiation (X-rays, cosmic rays, gamma rays)

36
Q

What is the result of using Nonionizing radiation (UV) vs using Ionizing radiation (X-rays, cosmic rays, gamma rays)?

A

UV radiation (Nonionizing): misread DNA sequence → call wrong base pair

Ionizing radiation (X-rays, cosmic rays, gamma rays): breaks → rearrangement/large deletions

37
Q

How do microorganisms try to fix their damaged DNA before cell division?

A

SOS System

38
Q

If the damaged DNA is repaired before cell division, will the mutation be passed on?

A

No

39
Q

When is the SOS System activated?

A

when DNA has considerable damage (lesions/breaks)

40
Q

When is the SOS System activated?

A

when DNA has considerable damage (lesions/breaks)

41
Q

What genes regulate SOS System?

A

RecA (activator) and LexA (repressor)

42
Q

How does the SOS System work?

A

System Activation
* DNA is damaged → RecA is expressed → RecA inactivates LexA → SOS System activated

Actual System
* Coordinated expression of proteins occur
* ex. DNA polymerase IV & DNA polymerase V enzymes
* Translesion synthesis: proteins bypass or ignore DNA lesions, para tuloy yung DNA replication

End of System
* After translesion synthesis → LexA is expressed → SOS System is repressed

43
Q

T/F

DNA polymerase IV & V are always very effective during the SOS System

A

F

DNA polymerase IV & V lacks proofreading → can cause even more mutations

Last Module Microbio Lec (6 decks)

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