I am on question G-I. Question 2: Population genetics of the Kermode black bear The Kermode Spirit bear is an alternate phenotype of the species Ursus americanus (black bear) in British Columbia that has striking white fur. It was determined in 2001 that a single nucleotide change from G to A results in the replacement of Tyrosine with Cysteine at codon 289 in the melanocortin 1 receptor gene ( mclr; Ritland et al. 2001 Current Biology). This allele ( W 2 ) is recessive to the wildtype allele ( W 1 ) , and occurs as a novel mutation in 1 out of every 10,000 copies. White phenotypes range in frequency from 10% to 25% on various islands, and have been present for long periods of time. Each island has approximately 50 individuals. It has been estimated that the white bears have a 20% advantage over black bears in fishing salmon from rivers due to decreased contrast with the sky. Assume these populations I started out initially as 100% WIWI (AA). A) Include a screenshot of the parameters used. (1 point) [paste output here] B) What evolutionary force(s) is/are acting on the W 2 allele? ( 1 point) [answer here] C) If selection, mutation, and drift were the only processes acting on these populations, what would be the eventual outcome(s) for the two alleles in a given population? (1 point) [answer here] D) Try running the simulation for fewer generations. How many generations does it take to fix a novel advantageous allele in all populations? What do these results suggest about the ability of selection to fix a novel advantageous mutation in a small population; in other words, why is selection "having trouble"? (1 point) [answer here] G) Rerun the simulation, changing the fitness of Aa so that W2 (a) is dominant. With a population size of 50 , how does the probability of the W 2 allele becoming fixed change if W 2 is the dominant allele as opposed to recessive? (1 point) [answer here] H) Why does this happen? (1 point) [answer here] I) Include the output and a screenshot of the parameters used. (1 point).

1. I am on question G-I.
Question 2: Population genetics of the Kermode black bear The Kermode Spirit bear is an
alternate phenotype of the species Ursus americanus (black bear) in British Columbia that has
striking white fur. It was determined in 2001 that a single nucleotide change from G to A results
in the replacement of Tyrosine with Cysteine at codon 289 in the melanocortin 1 receptor gene (
mclr; Ritland et al. 2001 Current Biology). This allele ( W 2 ) is recessive to the wildtype allele (
W 1 ) , and occurs as a novel mutation in 1 out of every 10,000 copies. White phenotypes range
in frequency from 10% to 25% on various islands, and have been present for long periods of
time. Each island has approximately 50 individuals. It has been estimated that the white bears
have a 20% advantage over black bears in fishing salmon from rivers due to decreased contrast
with the sky. Assume these populations I started out initially as 100% WIWI (AA). A) Include a
screenshot of the parameters used. (1 point) [paste output here] B) What evolutionary force(s)
is/are acting on the W 2 allele? ( 1 point) [answer here] C) If selection, mutation, and drift were
the only processes acting on these populations, what would be the eventual outcome(s) for the
two alleles in a given population? (1 point) [answer here] D) Try running the simulation for
fewer generations. How many generations does it take to fix a novel advantageous allele in all
populations? What do these results suggest about the ability of selection to fix a novel
advantageous mutation in a small population; in other words, why is selection "having trouble"?
(1 point) [answer here] G) Rerun the simulation, changing the fitness of Aa so that W2 (a) is
dominant. With a population size of 50 , how does the probability of the W 2 allele becoming
fixed change if W 2 is the dominant allele as opposed to recessive? (1 point) [answer here] H)
Why does this happen? (1 point) [answer here] I) Include the output and a screenshot of the
parameters used. (1 point)