Isci 350 Midterm

Front 1

What two claims are put forth by the theory of evolution?

Back 1

(1) species have changed over time

(2) new forms have arisen from common ancestors

Front 2

Provide evidence that species have changed through time (direct observation, there are 6)

Back 2

- peppered moths evolved in response to pollution (validated by experimental evidence)

- evolution of pesticide resistance (increase in # species resistant to pesticide)

- decrease in weight and horn length of bighorn rams due to hunting

- HIV evolved to be resistant to AZT

- Finches evolved deeper beaks following drought

- size of cod fish decreased due to fishing and then increased due to moratorium on fishing

Front 3

Provide evidence that species have changed through time (fossil records, there are 2)

Back 3

- transitional/intermediate forms of species

- lineage splitting in diatom Rhizosolenia

Front 4

Provide evidence that new forms have arisen from common ancestors

Back 4

Fossil record (intermediate forms between two species)

Direct observation (ring species of salamander)Homology (vestigial structures, embryological similarities, genetic homologies)

Front 5

What is the difference between homology and analogy?

Back 5

Homology: similarity due to shared ancestor, not necessarily functional (e.g. early embryonic development)

Analogy: similarity due to shared way of life (not due to common ancestor, e.g. panda's thumb)

Front 6

What are Darwin's four postulates of evolution by natural selection?

Back 6

1. TURNOVER: There needs to be multiple units that undergo death and reproduction

2. VARIABILITY: There must be variability among the units

3. HERITABILITY: Variation must be passed down from parents to offspring

4. DIFFERENTIAL REPRODUCTIVE SUCCESS: Some variants must be more likely to survive than others.

Front 7

What is the role of genetic drift?

Back 7

Neutral evolution and non-adaptive evolution, but also may act as a creative force to explore "rugged fitness landscapes". For example, the evolution of HIV from SIV had a relatively high fitness valley and adapted to humans easily.

Front 8

What are the three potential hypothesis for the evolutionary basis of disease symptoms?

Back 8

(1) adaptation of the host

(2) adaptation of the pathogen

(3) side effect of their interaction

Front 9

Describe the arms race between prey and predator

Back 9

If prey evolve traits to avoid detection from predator, predators evolve traits to better detect/hunt prey. This continues back and forth.

Front 10

What advantage do parasites and pathogens have over animals, and how have animals overcome this disadvantage?

Back 10

Pathogens and parasites have short life spans, huge population sizes, and high mutation rates. Animals have overcome this by evolving adaptive immunity.

Front 11

How do parasites/pathogens escape the attack from an adaptive immune system?

Back 11

e.g. african sleeping sickness - continual switching of surface antigens (variable surface glycoprotein, VSG)

e.g. influenza - antigenic drift: "changes to the flu virus that happen slowly over time". antigenic shift: when two strains recombine in the same cell.

Front 12

What is the problem of antibiotic resistance?

Back 12

Bacteria evolve very quickly, and the horizontal transfer of resistance factors, and compensatory mutations make up for cost of resistance

Front 13

How do fitness landscapes influence antibiotic resistance?

Back 13

In the absense of antibiotic, you'd expect pathogens to revert to wild (sensitive) type, but other mutations compensate for the cost of antibiotic resistance, creating a fitness valley that prevents that revertion.

Front 14

What does Ro represent, and what does it mean if it is above or below 1?

Back 14

Basic reproductive number. Mean # of secondary infections arising from one infected individual in a totally susceptible population.

If Ro > 1, then the disease is spreading. The larger it is, the harder it is to control.

Front 15

Define virulence, give example.

Back 15

reduction in lifetime reproductive success of host due to harm done by pathogen. e.g. over time, Myxoma virus became less virulent to rabbit population.

Front 16

How does mode of transmission affect virulence?

Back 16

1) vertical vs horizontal - opportunities for horizontal transmission increase virulence (e.g. fig wasps and parasitic nematodes)

2) direct vs vector tranmission - vector-based confers greater virulence

Front 17

How does opportunity for transmisison affect virulence?

Back 17

Behaviour of host and vector affect the likelihood that the parasite/pathogen infects an individual and spreads to others. As does the population structure and density.

Front 18

Factors affecting disease emergence

Back 18

1) opportunity for transmission between animal resevoir and humans (determined by animal/human contact, animal-animal contact)

2) opportunity for spread of new disease (human population structure/density)

Front 19

Factors affecting drug resistance

Back 19

1) Frequency/intensity/variety of drug use (overprescription, non-med use)

2) opportunity for transmission of antibiotic resistance factors + pathogens (in bodies, hospitals, public places)

Front 20

What are the 5 assumptions of the Hardy-Weinberg equilibrium?

Back 20

- no selection

- no mutation

- no migration

- random mating

- infinite population size

Front 21

In a HW equilirbium, given the frequency of both alleles, what is the frequency of each diploid combination of P and Q?

Back 21

PP = P^2

PQ or QP = 2PQ

QQ = Q^2

Front 22

How do you calculate expected equilibrium frequency of a recessive allele under mutation-selection balance?

Back 22

qˆ= sqrt(µ/s)

Front 23

Give two examples of heterozygote advantage

Back 23

1) Cystic fibrosis heterozygote might provide carriers resistance to typhoid, cholera, others.

2) Sickle-cell anemia: in normal regions, w (fitness) of ++ > w of S+. in malaria regions, Ws+>W++!

Front 24

Why hasn't natural selection eliminated genetic disease? (there are 5!)

Back 24

- Heterozygote advantage (e.g. CF, sickle-cell anemia) - Genetic drift/founder effect (e.g. Tay-Sachs, hereditary tyrosinemia) - Recurrent mutation with, perhaps, mutational bias (e.g. Huntington's) - Late onset (e.g. Huntington's) - Fitness tradeoff (equal or greater fitness prior to onset)

Front 25

How does the mutational bias affect the likelihood of a child being born with a Huntington's gene?

Back 25

number of repeats more likely to increase than decrease, and male sperm mutations increases with father's age

Front 26

Be able to calculate the expected frequency of an allele in a population given their fitnesses

Back 26

Ok :)

Front 27

Heritability?

Back 27

Go over the slides and write out the notes, it's not flashcard friendly!