Chapter 9 Flashcards

1
Q

How do we construct the history of a gene?

A

It is constructed like a tree, complete with the disadvantages of uncertainty. We reconcile this with incomplete lineage sorting, or using a lot of gene phylogenies to reconstruct a tree.

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2
Q

What is coalescence?

A

Related alleles being traced back to a common ancestor. They can help us understand divergence.

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3
Q

How do we deal with homoplasy when building a phylogeny with genetic data?

A

We use a lot of genetic characters in creating phylogenies. Slowly evolving genes to study distant species, rapidly evolving genes for closer ones. WE also use many genes or thousands of bases, which gains a lot of statistical power.

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4
Q

Adaptive evolution is…

A

common, and promotes beneficial mutations while removing detrimental ones. Selection operates more efficiently than drift.

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5
Q

Who is mitochondrial eve?

A

The one female ancestor who is the most recent common ancestor of all common humans. She was alive less than 250000 years ago. Ne then was 4600-11200.

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6
Q

What is the rate of neutral substitutions?

A

The rate of a new mutant fixing in a population and replacing whatever was there before.
prob of mutatant arising x prob that it fixes.
2Nμx 1/2n = μ

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7
Q

Increases in the mutation rate, U, will…

A

increase the rate of turnover and fixation, accelerating the molecular clock
increase the heterozygosity of the population

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8
Q

What are synonymous substitutions? (ks)

A

Amoni acid and protein function remains the same, evolves at a neutral rate, which depends on the mutation rate. Because these guys evolve under drift, they serve as a null hypothesis/control.

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9
Q

What are non-synonymous substitutions? (ka)

A

Amino acid sequence and properties of the protein change, and evolves more slowly than synonymous sites, which reflects purifying selection. When they evolve faster, they are evidence of positive selection.

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10
Q

Ks is….

A

The rate of DNA substitutions under no selection. In positive selection, it is smaller than Ka. In purifying, it is bigger, and evolution slows down.

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11
Q

What did McDonald and Kreitman do?

A

Developed a better test for detecting adaptive evolution from positive selection than the KA/KS test. It is the ratio of Ka to KS substitutions in the fixed differences between species. If selection was important, the KA/KS between species is bigger than the KA/KS within species. If drift causes the difference, then KA/KS = KA/KS. Only reveals positive selection, but is very powerful!

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12
Q

Why does the McDonald-Kreitman test use KA/KS ratio as a control?

A

Because most beneficial alleles fix quickly, mostly detrimental alleles are lost quickly, and alleles that stay polymorphic are largely neutral.

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13
Q

Positive and purifying selection…

A

leave distinctive genetic signatures.

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14
Q

What is linkage disquilibrium?

A

When alleles at different loci become associated with each other. An example is a new mutation arising randomly in a pop that automatically becomes associated with alleles at a nearby loci on the chromosome. This decays over time, which reflects crossovers and recombination.

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15
Q

What is evo-devo?

A

The genes driving development and diversification.

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16
Q

How do founder effects and genetic bottlenecks affect LD?

A

Populations that migrate farther experience an increase in LD due to repeated bottlenecks and selection.

17
Q

How are prokaryotic and eukaryotic genomes different? Why does this matter?

A

Prokaryotic #genes scales with size, whereas in eukaryotes, size does not predict #genes.
The first idea is that eukaryotes possibly needs this complexity because they have complex development and regulation.
The second idea is that eukaryotes are bigger, so they have smaller Ne which favors more drift and less selection.

18
Q

What happened at generation #33,100?

A

Gene duplication allowed a new function to evolve! This lets one copy free to evolve a new function. Commonly, a copy is inactivated.

19
Q

What are promiscuous proteins?

A

Proteins that can do more than one thing. They are especially likely to get new functions after duplicating.

20
Q

What do mutations in homeotic genes cause?

A

A displacement of structures, like legs in place of antennae in drosophila.

21
Q

What do hox genes do?

A

Determine where stuff is expressed during development. Shuffling them around fucks this up.

22
Q

What are paralogs?

A

Often resulting from gene duplication, they are gene families that occur within the same species. 2 copies of the same gene are called paralogs.

23
Q

What are orthologs?

A

Genes that diverge as species diverge.

24
Q

How does a gene gain a new function?

A

A gene duplicates. It can become inactivated (pseudogene) , free to evolve a new altered function (sub-functionalization) or can evolve a new function (neo functionalization)

25
Q

How do novel traits evolve?

A

From duplication and proteins being co-opted to serve other functions. Promiscuous proteins often provide a starting point for these novel traits.
They can arise when existing genes are expressed in new developmental contexts.

26
Q

Why do duplicated genes accumulate mutations rapidly?

A

Because they are free to evolve as they are released from purifying selection.

27
Q

How were snake forelimbs and hind legs dissapear?

A

Hind limbs were lost gradually from a decrease in Shh expression.
Forelegs were lost by expanding the range of the trunk anteriorly for hox gene expression.

28
Q

Do plants have genes similar to HOX genes?

A

Yes, they have KNOX genes. They are remarkably similar to the regulatory networks in animals.

29
Q

What does extopic activation of SHh cause?

A

A complex developmental cascade resulting in extra limbs.

30
Q

What are Dpp and BMP2 to each other?

A

They are orthologs, and examples of parallel evolution.

31
Q

Where did the similar proteins in eyes across lineages come from?

A

Opsins evolved from serpentine proteins, proteins that snake through a membrane, often receptors.. Crystallins evolved via gene recruitment.