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BIO3A: Processes 2 Patterns > S1: W1-W2 (Prof. Kelsey) > Flashcards

S1: W1-W2 (Prof. Kelsey) Flashcards

1
Q

Components of the biodiversity framework that we focus on? (4)

A

• Genes.
• Genetic structure & processes.
• Populations.
• Population structure.

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2
Q

Things to note when defining evolution & the variation that enables it? (3)

A

• Heritable change (gemline).
• Change due to imperfect DNA replication.
• Variation in success/fitness of variant/different DNA.

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3
Q

Macro-scale to micro-scale on the hierarchical nature on phylogenetic assessment? (2)

A

• Macro-scale deals with general taxa/animal groups.

• Micro-scale deals with detail within a group/taxon (pedigrees and stuff).

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4
Q

Difference between purines & pyramidines?

A

Purines have a double membrane while pyramidines have a single membrane.

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5
Q

Purines? (2)

A

• Adenine.
• Guanine.

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6
Q

Pyramidines? (2)

A

•Thymine.
• Cytosine.

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7
Q

Codon?

A

= a sequence of three nucleotide bases/letters in a DNA or RNA strand.

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8
Q

Central Dogma in Molecular Biology?

A

= unifying theme of evolutionary biology.

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9
Q

CDMB stands for?

A

Central Dogma in Molecular Biology.

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10
Q

CDMB components? (3)

A

• Replication.
• Transcription.
• Translation.

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11
Q

Replication?

A

= DNA is copied in cells.

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12
Q

Transcription?

A

= DNA is made into RNA expressed regions.

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13
Q

Translation?

A

= RNA is made into proteins, using DNA codons to select amino acids (mRNA, rRNA, tRNA).

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14
Q

Why is CDMB a unifying theme of evolutionary biology? (3)

A

• Enables nature’s flow of information (unidirectional flow).

• Used to identify individuals, populations & species.

• Study how changes to DNA alter biodiversity.

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15
Q

How does CDMB help to identify individuals, populations & species?

A

By different nucleotides being introduced at the same point during replication.

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16
Q

Locus/Loci?

A

= can be a gene or a neutral marker.

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17
Q

Genes attributes? (2)

A

• Have 2 alleles.
• Can be neutral markers.

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18
Q

Neutral marker attributes? (2)

A

• Multiple alleles.
• Not genes.

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19
Q

Microsatellite?

A

= short sequence of nucleotides repeated.

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20
Q

Monomorphic microsatellite?

A

= when the number of repeats is the same among individuals.

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21
Q

Polymorphic microsatellite?

A

= when the number of repeat varies between individuals.

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22
Q

Monomorphic microsatellite attribute?

A

• Not informative.

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23
Q

Polymorphic microsatellite attribute?

A

• Informative.

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24
Q

Where do genes come from? (3)

A

• Homology.
• Orthology.
• Paralogy.

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25
Q

Homology types? (2)

A

• Orthology.
• Paralogy.

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26
Q

Orthology?

A

= duplicates that share a common ancestor.

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27
Q

Paralogy?

A

= duplicates that don’t share a common ancestor.

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28
Q

Orthology attributes? (4)

A

• Related via speciation events.
• Within different species.
• Have similar functions.
• Retain original function.

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29
Q

Paralogy attributes? (4)

A

• Related via duplication event.
• Within the same species.
• Functions diverge.
• Evolves new function.

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30
Q

Why should we organize information with/using orthologs?

A

It’s because they enable one to find & compare data speedily.

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31
Q

Eg of paralogs?

A

Hox genes.

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32
Q

Why are duplicate genes important?

A

They provide a source of genetic material for mutation, drift and selection to act upon.

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33
Q

Why are paralogs helpful?

A

They provide useful information into the way genomes evolve.

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34
Q

Epistasis?

A

= gene-gene interaction.

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35
Q

Types of genes? (2)

A

• Structural/productive genes.
• Untranscribed genes.

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36
Q

Structural genes attributes? (2)

A

• Protein-coding genes.
• RNA-specifying genes.

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37
Q

Untranscribed genes attribute?

A

Non-functional.

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38
Q

Transcription factor?

A

= proteins involved in the process of transcribing/converting DNA into RNA.

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39
Q

Transcription factor functions? (2)

A

• Turn genes on/off.
• Regulate transcription of subsequent genes.

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40
Q

Intron?

A

= a nucleotide sequence that does not code for amino acids in a protein.

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41
Q

Eg of intron?

A

Neutral markers.

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42
Q

Why do introns make good neutral markers?

A

It’s because they are free to accumulate mutations at a higher rate than extrons with lower consequences.

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43
Q

Why do extrons make bad neutral markers?

A

It’s because they accumulate mutations at a slower rate than introns with higher consequences.

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44
Q

Genome types? (3)

A

• Nuclear DNA.
• Mitochondrial DNA.
• Chloroplast DNA.

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45
Q

Things to note when dealing with types of genomes? (3)

A

• Inheritance.
• ATP.
• Rubisco.

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46
Q

Chloroplast DNA vs Nuclear DNA vs Mitochondrial DNA regarding appearance?

A

• cpDNA = coiled.
• nDNA = round.
• mtDNA = round.

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47
Q

Chloroplast DNA vs Nuclear DNA vs Mitochondrial DNA regarding Inheritance?

A

• cpDNA = paternal.
• nDNA = maternal & paternal.
• mtDNA = maternal.

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48
Q

Barcode?

A

= unique gene region that work for a species.

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49
Q

Barcode uses? (3)

A

• Used for species identification.
• Provide evidence to refute/dispute morphological data.
• Help us understand biodiversity (Sting flowers).

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50
Q

Egs of barcodes? (3)

A

• tmK.
• tmS.
• trnL.

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51
Q

Cataloging life on earth using barcodes general process? (6)

A

• Collect specimen.
• Collect metadata.
• Tissue sample.
• DNA extraction.
• PCR amplification of DNA barcode.
• Sequencing of DNA barcode.

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52
Q

Polymerase Chain Reaction (PCR)?

A

= a method used to make many copies of a specific DNA region.

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53
Q

Kary Mullis?

A

= developed the method to amplify regions of DNA, automatically.

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54
Q

When was the PCR discovered?

A

1983.

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55
Q

List of PCR Reagents? (6)

A

• DNA.
• Primers.
• dNTPs (nucleotides As, Ts, Cs, Gs).
• Buffer.
• MgCl2.
• TAQ Polymerase.

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56
Q

DNA regarding PCR reagents?

A

= genomic/template.

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57
Q

Primers in terms of PCR reagents?

A

= identification region.

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58
Q

dNTPs in terms of PCR reagents?

A

= make new DNA.

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59
Q

Buffer in terms of PCR reagents?

A

= stabilizes reaction.

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60
Q

MgCl2 in terms of PCR reagents?

A

= enhance binding.

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61
Q

TAQ Polymerase in terms of PCR reagents?

A

= adds dNTPs to the template.

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62
Q

TAQ Polymerase attributes? (2)

A

• Found in the hot spring of a national park.
• Can handle really high temperatures (98°C) & performs optimally in this environment.

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63
Q

PCR main steps? (3)

A

• Denaturation of DNA & primers.
• Annealing a primer to template DNA.
• Elongation.

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64
Q

Temperature of Denaturing process of PCR?

A

95°C.

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65
Q

Temperature range of Annealing process of PCR?

A

45°C – 60°C.

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66
Q

Temperature of Elongation process in PCR?

A

72°C.

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67
Q

Why the Anealing temperature range?

A

It’s because the proportion of nucleotides (As, Cs, Ts, Gs) in your primer & DNA changes the temperature at which the primer will attach/anneal to your DNA successfully.

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68
Q

Low temperature in annealing = …?

A

Non-specific annealing.

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69
Q

High temperatures in annealing = …?

A

Specific.

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70
Q

Annealing step in PCR?

A

= process where primers bind to template DNA strands.

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71
Q

What does your PCR look like?

A

Gel electrophoresis image.

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72
Q

Types of molecular markers? (3)

A

• Single locus marker.
• Co-dominant & dominant markers.
• -Omics.

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73
Q

Process associated with single locus marker?

A

• Gene sequencing.

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74
Q

Process associated with co-dominant & dominant markers?

A

Fragment analyses.

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75
Q

Process associated with -omics marker?

A

Next genetic sequencing.

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76
Q

Molecular marker?

A

= a segment of DNA that is found at a specific location in a genome.

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77
Q

Gene sequencing?

A

= the ability to determine nucleotide sequences of DNA molecules.

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78
Q

Eg of Single locus marker?

A

Barcodes.

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79
Q

Gene sequencing uses? (2)

A

• Help you identify breeds (i.e., whether species are related).
• Used for DNA fingerprints.

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80
Q

Thing to note about gene sequencing & relatability?

A

If species relatability is >2%, it means that they are different species.

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81
Q

If a species >2% = …?

A

Different species.

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82
Q

Fragment analysis?

A

= the process of breaking down a DNA sample into various fragments using restriction enzymes, & visualizing and analyzing those fragments through the process of gel electrophoresis.

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83
Q

Dominant markers attributes? (3)

A

• Cannot distinguish between heterozygotes.
• Give inaccurate impression/lower estimate of genetic diversity.
• Represented as present or absent bands.

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84
Q

Why do dominant markers give a lower estimate of genetic diversity?

A

It’s because they mask the recessive gene.

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85
Q

Co-dominant markers attribute?

A

Can distinguish between heterozygotes.

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86
Q

Eg of Co-dominant markers?

A

Microsatellites.

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87
Q

Things to note regarding Microsatellites? (2)

A

• Way that fragment size changes is based on the number of repeats.
• Single locus has many alleles of different lengths.

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88
Q

Eg of Dominant markers?

A

DNA fingerprints.

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89
Q

-Omics markers attributes? (3)

A

• Blends concepts of single gene sequencing & fragment analysis.
• Parallel (simultaneous) sequencing of DNA fragments.
• Researchers sequence multiple regions of an organism’s genome.

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90
Q

Application of -Omics markers?

A

SNP.

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91
Q

SNP stands for?

A

Single Nucleotide Polymorphism.

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92
Q

SNP?

A

= variation in a DNA sequence occurring when a single nucleotide in a genome is altered.

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93
Q

Molecular markers uses? (5)

A

• Genetic variation.
• Species identification.
• Invasion biology.
• Disease ecology.
• Identifying genetic conditions, viruses & other medical conditions.

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94
Q

How are molecular markers used in genetic variation? (2)

A

Via:

• Population structure.
• Evolution.

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95
Q

How are molecular markers used in Species identification? (2)

A

Via:

• Taxonomy.
• Systematics.

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96
Q

How are molecular markers used in Invasion biology?

A

Biocontrol.

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97
Q

How are molecular markers used in Disease Ecology? (2)

A

Via:

• Genetic predisposition/susceptibility.
• Infection routes.

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98
Q

How are molecular markers used in identifying genetic conditions, viruses, etc? (2)

A

Via:

• Medical practice.
• Genetic counseling.

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99
Q

Important thing to note of molecular markers?

A

Must not be under selection (i.e., must be in HWE).

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100
Q

Why must molecular markers not be under selection?

A

It’s because they are “neutral” regions of genomes.

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101
Q

How do you tell if something is under selection?

A

It is not in HWE.

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102
Q

Why are neutral markers important?/Why do you think you need neutral markers?

A

Shifts your view of genetic variation:

  • If a marker is neutral, you get a good estimate of variation.
  • If a marker is under selection, it is bad for variation.
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103
Q

Main causes of genetic variation? (2)

A

• Recombination.
• Mutations.

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104
Q

Recombination?

A

= the shuffling of genes (alleles) between chromosomes.

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105
Q

Mutation?

A

= heritable changes in genetic information.

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106
Q

External causes of mutations? (2)

A

• “Naturally” occurring causes.
• External influences.

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107
Q

Egs of external influences? (3)

A

• Sun.
• Chemicals.
• Radiation.

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108
Q

What happens when DNA mutates? (4)

A

• Nothing (it’s a neutral/synonymous mutation).
• Advantageous.
• Deleterious.
• Conservative.

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109
Q

Advantageous effect if a DNA mutates attributes? (2)

A

• Increases fitness.
• Rare.

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110
Q

Deleterious effect if a DNA mutates attributes? (2)

A

• Common.
• Changes gene function/shuts off your genes.

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111
Q

Eg of a Deleterious effect of a DNA mutating?

A

BRCA1.

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112
Q

Conservative effect when a DNA mutates?

A

= a change in amino acids but the new amino acid has similar chemical properties (doesn’t change much).

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113
Q

Types of mutations? (4)

A

• Point mutations.
• Indels.
• Frameshifts.
• Macromutations.

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114
Q

Point mutation?

A

= nucleotide substitutions (where one base is changed to a different base).

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115
Q

Types of point mutations? (3)

A

• Silent.
• Non-sense.
• Mis-sense.

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116
Q

Silent point mutation?

A

= muation where a single nucleotide base is changed, but that change does not affect the amino acid sequence.

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117
Q

Non-sense point mutation?

A

= mutation that changes an amino acid to a stop codon.

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118
Q

Mis-sense point mutation?

A

= point mutation where a single nucleotide is changed, resulting in a codon that codes for a different amino acid.

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119
Q

Types of Mis-sense point mutations? (2)

A

• Conservative.
• Non-conservative.

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120
Q

Silent point mutation illustration? (3)

A

● DNA level = TTC [to TTT]
● mRNA level = AAG [to AAA]
● Protein level = Lys [to Lys]

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121
Q

Non-sense point mutation illustration? (3)

A

● DNA level = TTC [to ATC]
● mRNA level = AAG [to UAG]
● Protein level = Lys [to STOP]

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122
Q

Conservative Mis-sense point mutation illustration? (3)

A

● DNA level = TTC [to TCC]
● mRNA level = AAG [to AGG]
● Protein level = Lys [to Arg]

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123
Q

Non-conservative Mis-sense point mutation illustration? (3)

A

● DNA level = TTC [to TGG]
● mRNA level = AAG [to ACG]
● Protein level = Lys [to Thr]

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124
Q

Egs of Mis-sense point mutations? (3)

A

• ALS (Amyotrophic Lateral Sclerosis).
• Cystic fibrosis.
• Sickle cell anaemia.

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125
Q

Indel mutation?

A

= mutation where larger gaps are deleted or inserted into a DNA sequence.

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126
Q

Important thing to note about Indel mutation?

A

They are much harder to predict in evolutionary models.

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127
Q

Why are Indel mutations harder to predict in evolutionary models?

A

It’s because we have to think about the homology of the nucleotides that are left in the gaps (parsimony).

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128
Q

Frameshift mutation?

A

= mutation that causes a shift in the reading frame of the genetic message.

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129
Q

Effect of a frameshift mutation?

A

Alters the protein tremendously.

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130
Q

Frameshift mutation illustration?

A

● Original = The fat cat sat
● Mutated = hef atc ats at

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131
Q

Macromutations?

A

= large changes in gene regions (sometimes due to recombination).

132
Q

Macromutations attributes? (2)

A

• Happen on chromosome level.
• Polyploidy-genome duplication.

133
Q

What causes polyploidy-genome duplication?

A

Non-disjunction.

134
Q

Eg of Macromutations?

A

Tragopogon (goat’s beard).

135
Q

Explain eg of Macromutations?

A

Pieces of chromosomes translocate (mixed colour chromosome).

136
Q

Type of Macromutations?

A

Aneuploidy.

137
Q

Aneuploidy?

A

= the gaining/losing of a chromosome.

138
Q

Polyploidy?

A

= the gaining/losing of a whole set of chromosomes.

139
Q

Do mutations have patterns?

A

Yes.

140
Q

How is it that mutations have patterns? (2)

A

• Mutations are accumulated non-randomly (predictable).
• G & C mutate more readily than A & T.

141
Q

Eg of where patterns of mutations are observed?

A

Tarsir’s genome (where transitions are more common than transversions).

142
Q

Types of Nucleotide substitutions? (2)

A

• Transition.
• Transversion.

143
Q

Transition?

A

= when a purine converts to a purine, or a pyrimidine converts to a pyrimidine.

144
Q

Transversion?

A

= when a purine converts to a pyrimidine, or pyrimidine to a purine.

145
Q

Why are transition & transversion important when thinking about protein coding genes?

A

To enable us to predict the downstream effects, especially of transversion.

146
Q

Why do we conduct evolutionary analyses? (6)

A

• Better understand evolutionary effects of mutations.
• Identify closely related sequences or genes.
• Understand gene families & function.
• Consider evolutionary history of a species.
• Identify genes under selection.
• Estimate the timing of variation & evolution.

147
Q

Explain what you mean that we conduct evolutionary analyses to understand genes families & function?

A

That we get better ideas of gene relatability.

148
Q

What do you mean that we conduct evolutionary analyses to estimate the timing of variation & evolution?

A

We mean that we can date phylogenies.

149
Q

How do mutations help us understand the evolutionary implications of variation?

A

By generating the genetic variation that evolutionary processes depend on to act on organisms.

150
Q

What is the 3rd position of a codon called?

A

Wobble.

151
Q

Why is the 3rd position of a codon called a wobble?

A

It’s because it can change but the codon can still.produce the same protein.

152
Q

Which position(s) of a codon undergo strong selection?

A

1st & 2nd positions of a codon.

153
Q

Thing to note about the 3rd position of a codon?

A

Undergoes a high rate of mutation.

154
Q

Rate?

A

= change over time.

155
Q

Why is there rate variation among regions? (3)

A

• Nucleotide substitutions
• Pseudogenes.
• Each codon changes differently over time.

156
Q

Pseudogenes?

A

= non-functional fragments of DNA that resemble a functional gene.

157
Q

Pseudogenes attributes? (2)

A

• Free to change.
• Have a high rate of variation.

158
Q

Why do Pseudogenes have a high rate of variation?

A

It’s because they are not under strong selection.

159
Q

Factors affecting genetic diversity? (4)

A

• Mutation.
• Genetic drift.
• Inbreeding.
• Gene flow.

160
Q

Types of genetic variation? (2)

A

• Neutral.
• Adaptative.

161
Q

Neutral genetic variation?

A

= where there’s no selective advantage/disadvantage.

162
Q

Eg of Neutral genetic variation?

A

Eye colour.

163
Q

Adaptive genetic variation?

A

= where there’s a selective advantage/disadvantage.

164
Q

Egs of Adaptive genetic variation? (2)

A

• Venom.
• Darwin’s finches.

165
Q

Hierarchical organization of genetic diversity? (bottom to top) [4]

A

Within individual
|
Individual
|
Within populations
|
Among populations

166
Q

Implications of genetic variation/diversity within populations? (3)

A

• Critical factor in population/species survival.
• High chances for survival as environment changes.
• Small, isolated populations are less likely to survive drastic/any change.

167
Q

Why are small, isolated populations less likely to survive drastic/any change?

A

It’s because of low genetic variation & decreased drift.

168
Q

Genetic diversity/variance among populations use?

A

Help us think about how populations are changing through time.

169
Q

Why is genetic variation/diversity high among populations?

A

It’s because of various evolutionary processes such as NS, mutations & genetic drift.

170
Q

Implication of genetic diversity/variation among populations?

A

Population divergence/structuring.

171
Q

Use of population divergence/structuring?

A

Helps you to figure out where diverge took place.

172
Q

Contributors to population divergence/structuring? (2)

A

• Co-adapted gene complexes.
• Speciation.

173
Q

Co-adapted gene complexes?

A

= set of alleles/genes that increase the fitness in a specific environment.

174
Q

Genetic diversity within populations attributes? (5)

A

• High gene flow.
• High mutations.
• Decreased NS.
• Decreased genetic drift.
• Decreased inbreeding.

175
Q

Genetic diversity among populations attributes? (4)

A

• High NS.
• High genetic drift.
• High mutations.
• Decreased gene flow.

176
Q

Eg of Hierarchical organization of genetic diversity?

A

Tragopogon miscellus.

177
Q

Genetic diversity within individual attributes?

A
178
Q

Genetic diversity in individual attributes?

A
179
Q

Explain Elongation process of PCR?

A

It’s where DNA polymerase (TAQ) is used to extend the DNA fragment between the primers.

180
Q

Desirable properties for molecular markers? (5)

A

• Polymorphism.
• Co-dominant inheritance•••

181
Q

Egs of Frameshift mutations? (2)

A

• Insertions.
• Deletions.

182
Q

What do Macromutations include? (4)

A

• Deletions.
• Duplications.
• Translocations.
• Inversions.

183
Q

Deletion (chromosomal)?

A

= loss of all or part of a chromosome.

184
Q

Duplication (chromosomal)?

A

= produces an extra copy of all or part of a chromosome.

185
Q

Inversion (chromosomal)?

A

= reverses the direction of parts of a chromosome.

186
Q

Translocation?

A

= occurs when part of one chromosome breaks off and attaches to another.

187
Q

What causes a Frameshift mutation?

A

Insertion or deletion.

188
Q

Types of molecular markers? (2)

A

• Neutral markers.
• Adaptive markers.

189
Q

Genetic diversity/variation hierarchy? (3)

A

• Individual.
• Among individuals within populations.
• Among populations.

190
Q

What do evolution analyses depend on?

A

Rate of mutation (eg substitutions).

191
Q

Evolutionary analyses uses? (4)

A

• Help us estimate the timing of divergence.
• Help us estimate selection on on genes & populations.
• History of biodiversity.
• Evolutionary history of species, populations & genes/gene regions.

192
Q

Rate attributes?

A

• vary within & among organisms, genes, regions of genes & nuclear vs organellar genomes (mtDNA & cpDNA).

193
Q

1st codon position name?

A

Non-degenerate sites.

194
Q

2nd codon position name?

A

Twofold degenerate sites.

195
Q

3rd codon position name?

A

Fourfold degenerate sites.

196
Q

COVID-19 mutation rates?

A

An eg of where a gene has a different rate than the whole genome.

197
Q

Eg of Point mutation in general?

A

SNP.

198
Q

Why should we model evolution? (4)

A

• Describes the changes of fixed mutations.
• Amount of change, i.e., function of time since divergence.
• Incorporate what we know about rates of change.
• Estimate genetic differences or similarities.

199
Q

Substitution model assumptions? (3)

A

• Sites (A,T,G,C) are independent of each other & site homogeneity.
• Current base & future substitutions are independent of the past (no relationship).
• Temporal homogeneity (mutations occur per unit time).

200
Q

Note about Substitution model assumptions?

A

Only apply to gene regions that are not undergoing selection (i.e., neutral markers).

201
Q

Foundation of models?

A

Each p = probability of a change between the 2 nucleotides & 12 independent probabilities have to be considered.

202
Q

List models of evolution? (4)

A

• Jukes-Canter model (JC).
• Kimura 2-parameter model (K2P).
• Hasegawa-Kishino-Yano 85 model (HKY85).
• General Time Reversable model (GTR).

203
Q

Jukes-Canter (JC) model attributes? (5)

A

• Simplest model.
• One parameter (mu).
• Equal base frequencies (0.25).
• Assumes a single rate of change among nucleotides.
• Equal probabilities (mu).

204
Q

JC scenarios?

A

EG1 EG2
t=0 A A
t=1 A Not A
t=2 A A

Therefore, in EG2 we lost information because we don’t know what nucleotide was changed.

205
Q

K2P model attributes? (5)

A

• 2 parameters (mu & beta).
• Equal base frequencies (0.25).
• 1 parameter for transitions (alpha).
• 1 parameter for transversions (beta).
• Different probabilities of

206
Q

K2P scenarios?

A

EG1 EG2 EG3 EG4
t=0 A A A A
t=1 A G C T
t=2 A A A A

Therefore, in EG2 you have transition (alpha), EG3 you have transversion (beta), EG4 you have transversion (beta).

207
Q

HKY85 model attributes? (3)

A

• Unequal base frequencies.
• Account for transition/transversion rate difference (K = alpha / beta).
• Put nucleotides in a matrix as each has a different base frequency.

208
Q

Why put nucleotides in a matrix?

A

It’s because each nucleotide has a different base frequency.

209
Q

GTR model attributes? (3)

A

• Unequal base frequencies (meaning 4 equilibrium base frequencies).
• Allows all 6 substitutions to have different rates.
• Each nucleotide has its own probability.

210
Q

What do we mean when we say it allows for all 6 substitutions to have different rates?

A

We mean that you now have different rates for different transitions & different rates for different transversions, which ALL have different probabilities.

211
Q

What do we mean by 4 equilibrium base frequencies?

A

We mean that each nucleotide has an equilibrium frequency.

212
Q

What to think about when dealing with models of evolution? (2)

A

• Base frequencies (whether they’re equal or not).
• Substitutions & their rates (are substitution rates equal).

213
Q

Why do we use models of evolution?

A

• Help us calculate genetic distance.

214
Q

Genetic distance?

A

= estimate of the amount of genetic divergence between sequences/microsatellite regions.

215
Q

Genetic distance AKA?

A

Net nucleotide distance.

216
Q

How do we calculate genetic distance? (4)

A

● Use sequence data.
● Count no. of subs / total #sites.
● Use a model of evolution to estimate substitutions.
● Interpret data.

217
Q

How to interpret the data after calculating genetic distance? (3)

A

• Range is 0 to 1.
• Lower values = sequences are more similar to each other.
• Higher values (closer to 1) = sequences are different from each other.

218
Q

Sequence data vs Microsatellites?

A

● Sequence data
= deals with substitutions.

● Microsatellite
= deal with allele frequencies (presence/absence in sample).

219
Q

Genetic distance uses?

A

Estimate population diversity.

220
Q

Genetic distance uses?

A

Estimate population diversity.

221
Q

Stepwise mutation model use?

A
222
Q

Infinite allele model?

A

= model that allows for more microsatellites in any direction.

223
Q

Types of genetic distance?

A

• Heterozygosity.

224
Q

Heterozygosity attributes? (3)

A

• Based on alleles (haplotype for sequences).
• Observed vs expected heterozygosity.
• Locus, individual & population variation.

225
Q

Things to look for when interpreting heterozygosity estimates (“summary statistics” in genetics)? [2]

A

• Site = nucleotide = position in sequence.
• HsubscriptE = heterozygosity (consider the evolutionary processes contributing to this).

226
Q

Evolutionary processes that affect genetic variation/diversity? (4)

A

• Mutation.
• Gene flow.
• Drift.
• Selection.

227
Q

Which evolutionary processes that affect genetic diversity increases heterozygosity? (3)

A

• Mutations.
• Gene flow.
• Selection.

228
Q

Which evolutionary processes that affect genetic diversity decreases heterozygosity? (2)

A

• Drift.
• Selection.

229
Q

Which evolutionary processes that affect genetic diversity increases differentiation? (3)

A

• Mutation.
• Drift.
• Selection.

230
Q

Which evolutionary processes that affect genetic diversity decreases differentiation? (2)

A

•Gene flow.
• Selection.

231
Q

Which evolutionary processes that affect genetic diversity affect all loci equally? (2)

A

• Gene flow.
• Drift.

232
Q

Which evolutionary processes that affect genetic diversity DON’T affect all loci equally? (3)

A

• Mutation.
• Selection.

233
Q

Why do mutation & selection not affect all loci equally?

A

It’s because they are loci-specific & therefore a change in locus can happen in 1 individual but not the other.

234
Q

Why do gene flow & drift affect all loci equally?

A

It’s because they happen in individuals & therefore in all of the loci.

235
Q

Difference between neutral markers & adaptive markers regarding location?

A

● Neutral markers
= on gene regions.

● Adaptive markers
= on genes.

236
Q

G

A
237
Q

Where do we apply the

A
238
Q

Types of balances? (2)

A

• Mutation-selection balance.
• Migration-selection balance.

239
Q

Mutation-selection balance?

A

= where because most mutations are deleterious, selection tries to eliminate them but cannot due to mutations having higher frequencies than selection can act on.

240
Q

How/In what ways do mutations remain in populations? (2)

A

• Heterozygotes (via masking of deleterious mutation).
• Drift.

241
Q

How does genetic drift ensure that deleterious mutations stay in the population?

A
242
Q

Egs of Mutation-selection balance? (2)

A

• Waser & Price (1981) with Delphinium melsonii.
• Cystic fibrosis.

243
Q

Explain Waser & Price (1981)? (2)

A

● Found that pollinators didn’t visit white morphs of Delphinium melsonii but these morphs persisted even though they had low fitness.

● Selection couldn’t act on it as some pollinators were still visiting some of the white morphs.

244
Q

Explain Cystic fibrosis?

A

• Caused by mutations in the CFTR gene and was selected against because males with it are infertile.

245
Q

Cystic fibrosis?

A

= condition where you have autosomal recessive inheritance.

246
Q

Migration-selection balance?

A

= where local adaptation in subpopulations is caused by selection & migrated by migration.

247
Q

Migration-selection balance attributes? (3)

A

• Movement of alleles balances out selective pressures.
• Differentiation occurs if s>m (i.e., if selection is overpowering migration).
• Differentiation ONLY at the loci affecting traits that selection is acting on (the single trait).

248
Q

Symbols in s>m?

A

• s = selection coefficient across subpopulations.
• m = fraction of migrants each generation.

249
Q

Egs of Migration-selection balance? (2)

A

• Industrial melanism is moths.
• Snake venom.

250
Q

Explain Industrial melanism in moths? (2)

A

• Local adaptation occurred.
• Selection acted stronger than migration.

251
Q

Explain Snake venom?

A

Dietary needs is what caused the change in the venom.

252
Q

Migration & drift in terms of Migration-selection balance?

A

Because most alleles are lost in small populations through drift, new alleles are replaced through migrants to balance it out.

253
Q

Equation for Migration & Drift in terms of Migration-selection balance?

A

Fsub(ST) = 1/ (1+4Ne m)

254
Q

Symbols of Migration & Drift relating to Migration-selection balance? (3)

A

• Ne = effective population size.
• m = migrant.
• Fsub(ST) = population differentiation.

255
Q

Fsub(ST) attributes? (2)

A

• How different your populations are.
• Takes into account how Ne (population size) is different from migrants.

256
Q

Ne?

A

Tells you about drift.

257
Q

Drift effect on subpopulation differentiation?

A

Increases differentiation among subpopulations.

258
Q

Migration effect on subpopulation differentiation?

A

Decreases differentiation among subpopulations.

259
Q

Selection & Drift in terms of Migration-selection balance?

A

In order for for selection to counteract drift in small populations, it needs to be much stronger (high s).

260
Q

Thing to consider for Migration-selection balance?

A

Migration & selection try to counteract drift effects in small populations. Migration counteracts it by bringing in new alleles, while selection counteracts it by acting strongly on them.

261
Q

When does selection determine allele frequency?

A

When:

s > 1/2Ne.

262
Q

1/2Ne?

A

= rate of genetic drift.

263
Q

Eg of Selection in drift?

A

Purple loosestrife flowers.

264
Q

Explain Purple loosestrife flowers?

A

3 morphs (long style, mid style, short style) are maintained by negative frequency dependent selection, but morphs can be lost in small populations due to drift.

265
Q

How do populations survive changing environments (adapt)? (3)

A

• Dispersal.
• Phenotypic plasticity.
• Adaptation.

266
Q

Focus is on…?

A

Adaptation.

267
Q

Why do we need to consider genetics in understanding selection on phenotypes?

A

It’s because genetics are underlying mechanisms of phenotypes.

268
Q

Adaptation in terms of genetic basis attributes? (3)

A

• Can drive increase or decrease in genetic distribution.
• One genotype can produce multiple phenotypes.
• Multiple genotypes can produce one phenotype.

269
Q

Eg of where one genotype produces multiple phenotypes?

A

Daphnia species having helmets in the presence of predators & no helmets in their absence.

  • Helmet = phenotype.
270
Q

Eg of multiple genotypes producing one phenotype?

A

Tetrahymena (is an eg of Phenotypic parallelism, which overrides genetic divergence).

271
Q

Genetic basis of adaptation questions asked? (2)

A

• Does adaptation involve 1 gene or multiple genes?
• Are the same genes involved in adaptations across diverse groups?

272
Q

Eg of genetic basis of adaptation?

A

Antarctic ice fishes (Nototheinoid fishes) & Arctic Gadids.

273
Q

Explain Nototheinoid fishes & Arctic Gadids? (3)

A

• Partial de novo gene evolution.
• Both fish have anti-freeze protein (AFGP).
• Essentially, scientists “turned” on an unrelated ancestral gene to a functional gene in Arctic gadids (hence the de novo evolution).

274
Q

Things to consider in terms of genetic variation & adaptive potential? (3)

A

• How genetic variation is related to fitness.
• Populations genetic composition (allele/haplotype frequencies).
• Measuring the fitness of variable phenotypes.

275
Q

What is key for adaptive potential? (2)

A

• Fitness.
• Diversity.

276
Q

Egs under Genetic variation & adaptive potential? (2)

A

• Geospiza finches.
• Opposum shrimp.

277
Q

Opposum shrimp attributes? (2)

A

• Model organism for conservation genetics in changing environments.
• Tells us that genetic diversity is important in changing environments.

278
Q

What enables diversity for adaptation?

A

Adaptive markers!

279
Q

Adaptive marker?

A

= gene/DNA region that’s under selection.

280
Q

What can you use to identify adaptive markers? (2)

A

• Genomics.
• Controlled crosses approach.

281
Q

Controlled crosses approach attributes? (3)

A

• Help you figure out the proportion of phenotypes, which in turn helps you link it to gene region.
• Often needs whole genome coverage.
• SNPs.

282
Q

Eg of adaptive markers?

A

Mimmulus flowers.

283
Q

Egs of gene families used to quantify adaptive genetic diversity? (2)

A

• MHC genes.
• S loci.

284
Q

What do we use to quantify adaptive genetic diversity?

A

Gene families.

285
Q

How do we test for adaptations & gene differentiation? (3)

A

Use a combination of marker types & look for patterns of selection:

• Neutral markers.
• Adaptive markers.
• Sequence data.

286
Q

Neutral marker in testing for adaptations & genetic differentiation?

A

Show similar levels of genetic divergence (low divergence).

287
Q

Adaptive marker in testing for adaptations & genetic differentiation?

A

Show variable (anomalous) levels of divergence.

288
Q

Sequence data in testing for adaptations & genetic differentiation?

A

Compare non-synonymous & synonymous substitutions.

289
Q

Egs of testing for adaptations & genetic differentiation? (2)

A

• Stickleback fish.
• Mimmulus.

290
Q

Explain Stickleback fish?

A

Genome scan of 45 000 SNPs indicates genomic differences between freshwater populations.

291
Q

Explain Mimmulus? (2)

A

• Indicates genetic discordance.
• Where although other flowers are annual or perennial, this flower tends to be both annual & perennial.

292
Q

Selection patterns that indicate adaptation? (2)

A

• Directional selection.
• Stabilizing selection.

293
Q

Directional selection effects? (2)

A

• Increases population differentiation.
• Decreases

294
Q

Stabilizing selection effects? (2)

A

• Decreases population differentiation.
• Increases

295
Q

What is used to estimate selection?

A

Molecular data (protein coding genes & dN/ds ratio).

296
Q

dN/ds ratio?

A

= proportion of non-synonymous to synonymous substitutions.

297
Q

How do we calculate selection with molecular data?

A

Z-test.

298
Q

Z-test Ho (null hypothesis)?

A

Ho: dN = ds.

299
Q

Z-tedt HA (alternate hypothesis)? (3)

A

• dN = ds
• dN > ds
• dN < ds

300
Q

dN = ds means…?

A

Test of neutrality.

301
Q

dN > ds means…?

A

Positive selection.

302
Q

dN < ds means…?

A

Purifying selection.

303
Q

Positive selection means…?

A

Non-synonymous substitutions favoured.

304
Q

Purifying selection means…?

A

Non-synonymous substitutions selected against.

305
Q

Are changes in traits due to selection or drift?

A

Ho & Smith 2016 paper.

306
Q

Summarize Ho & Smith 2016 paper?

A
307
Q

If dN/ds ratio is close to 1?

A

Positive selection.

308
Q

If dN/ds is close to 0?

A

Purifying selection.

309
Q

Consequence of adaptation?

A

Isolation.

310
Q

Eg of a consequence of adaptation?

A

White & purple flowers where bees pollinated the purple flowers & the white flowers were isolated.

311
Q

How does adaptation drive genetic differentiation?

A

Populations ar the periphery tend to have low genetic diversity & high differentiation as a consequence of selection.

312
Q

Eg of adaptation driving genetic differentiation?

A

Malaria mosquitoes.

313
Q

Explain Malaria mosquitoes?

A

• Inversion is being selected for by the environment they live in.
• Dagilis & Kirkpatuck, 2016 & Ayala et al, 2013 papers.

314
Q

Ayala et al, 2013 paper summary?

A
315
Q

Dagilis & Kirkpatuck, 2016 paper summary?

A
316
Q

Why do we use adaptive markers?

A

To examine inbreeding depression on populations.

317
Q

Hypotheses for inbreeding depression? (2)

A

• Dominance.
• Overdominance.

318
Q

Dominance hypothesis?

A

= where there’s unmasking of deleterious alleles through a reduction of heterozygotes.

319
Q

Overdominance attributes? (2)

A

• Where you have heterozygote advantage.
• Increase in homozygotes = less fit heterozygotes.

320
Q

What do we use to test which of the mechanisms in the competing hypotheses are prominent?

A

Adaptive markers.

321
Q

Eg of inbreeding depression?

A

Drosophila.

322
Q

Explain Drosophila in inbreeding depression? (2)

A

• Heat shock genes were upregulated in inbred Drosophila when they were exposed to high temperatures.
• Inbreeding acted as an environmental stressor.

323
Q

Speed of inbreeding & adaptation?

A

Demontis et al, 2007 paper.

324
Q

Explain Demontis et al, 2007 paper?

A
325
Q

What represents the no. of subs when using sequence data to calculate genetic distance?

A
326
Q

What represents the total # of sites when using sequence data to calculate genetic distance?

A

BIO3A: Processes 2 Patterns (12 decks)

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