Assume that the flower population described in the previous problem undergoes a different pattern of predation. Flower-color determination and the starting frequencies of C₁ and C₂ are as described above, but the new insects attack yellow and red flowers, not orange flowers. As a result of the predation pattern, the relative fitness values are C₁C₁ = 0.40, C₁C₂ = 1.0, and C₂C₂ = 0.80.
What are the allele frequencies after one generation of natural selection?

In a population of flowers growing in a meadow, C₁ and C₂ are autosomal codominant alleles that control flower color. The alleles are polymorphic in the population, with f(C₁) = 0.80 and f(C₂) = 0.20. Flowers that are C₁C₁ are yellow, orange flowers are C₁C₂, and C₂C₂ flowers are red. A storm blows a new species of hungry insects into the meadow, and they begin to eat yellow and orange flowers but not red flowers. The predation exerts strong natural selection on the flower population, resulting in relative fitness values of C₁C₁ = 0.30, C₁C₂ = 0.60, and C₂C₂ = 1.0.

Assuming the population begins in H-W equilibrium, what are the allele frequencies after one generation of natural selection?

In a population of flowers growing in a meadow, C₁ and C₂ are autosomal codominant alleles that control flower color. The alleles are polymorphic in the population, with f (C₁) = 0.80 and f (C₂) = 0.20. Flowers that are C₁C₁ are yellow, orange flowers are C₁C₂, and C₂C₂ flowers are red. A storm blows a new species of hungry insects into the meadow, and they begin to eat yellow and orange flowers but not red flowers. The predation exerts strong natural selection on the flower population, resulting in relative fitness values of C₁C₁ = 0.30, C₁C₂ = 0.60, and C₂C₂ = 1.0.

Assuming random mating takes place among survivors, what are the genotype frequencies in the second generation?

In a population of flowers growing in a meadow, C₁ and C₂ are autosomal codominant alleles that control flower color. The alleles are polymorphic in the population, with f (C₁) = 0.80 and f (C₂) = 0.20. Flowers that are C₁C₁ are yellow, orange flowers are C₁C₂, and C₂C₂ flowers are red. A storm blows a new species of hungry insects into the meadow, and they begin to eat yellow and orange flowers but not red flowers. The predation exerts strong natural selection on the flower population, resulting in relative fitness values of C₁C₁ = 0.30, C₁C₂ = 0.60, and C₂C₂ = 1.0.

If predation continues, what are the allele frequencies when the second generation mates?

Assume that the flower population described in the previous problem undergoes a different pattern of predation. Flower-color determination and the starting frequencies of C₁ and C₂ are as described above, but the new insects attack yellow and red flowers, not orange flowers. As a result of the predation pattern, the relative fitness values are C₁C₁ = 0.40, C₁C₂ = 1.0, and C₂C₂ = 0.80.

What are the genotype frequencies among the progeny of predation survivors?

Assume that the flower population described in the previous problem undergoes a different pattern of predation. Flower-color determination and the starting frequencies of C₁ and C₂ are as described above, but the new insects attack yellow and red flowers, not orange flowers. As a result of the predation pattern, the relative fitness values are C₁C₁ = 0.40, C₁C₂ = 1.0, and C₂C₂ = 0.80.

What are the equilibrium allele frequencies in the predation environment?

ABO blood type is examined in a Taiwanese population, and allele frequencies are determined. In the population, f (Iᴬ) = 0.30, f (Iᴮ) = 0.15, and f (i) = 0.55.f. Assuming Hardy–Weinberg conditions apply, what are the frequencies of genotypes, and what are the blood group frequencies in this population?

A form of dwarfism known as Ellis–van Creveld syndrome was first discovered in the late 1930s, when Richard Ellis and Simon van Creveld shared a train compartment on the way to a pediatrics meeting. In the course of conversation, they discovered that they each had a patient with this syndrome. They published a description of the syndrome in 1940. Affected individuals have a short-limbed form of dwarfism and often have defects of the lips and teeth, and polydactyly (extra fingers). The largest pedigree for the condition was reported in an Old Order Amish population in eastern Pennsylvania by Victor McKusick and his colleagues (1964). In that community, about 5 per 1000 births are affected, and in the population of 8000, the observed frequency is 2 per 1000. All affected individuals have unaffected parents, and all affected cases can trace their ancestry to Samuel King and his wife, who arrived in the area in 1774. It is known that neither King nor his wife was affected with the disorder. There are no cases of the disorder in other Amish communities, such as those in Ohio or Indiana.

From the information provided, derive the most likely mode of inheritance of this disorder. Using the Hardy–Weinberg law, calculate the frequency of the mutant allele in the population and the frequency of heterozygotes, assuming Hardy–Weinberg conditions.

A form of dwarfism known as Ellis–van Creveld syndrome was first discovered in the late 1930s, when Richard Ellis and Simon van Creveld shared a train compartment on the way to a pediatrics meeting. In the course of conversation, they discovered that they each had a patient with this syndrome. They published a description of the syndrome in 1940. Affected individuals have a short-limbed form of dwarfism and often have defects of the lips and teeth, and polydactyly (extra fingers). The largest pedigree for the condition was reported in an Old Order Amish population in eastern Pennsylvania by Victor McKusick and his colleagues (1964). In that community, about 5 per 1000 births are affected, and in the population of 8000, the observed frequency is 2 per 1000. All affected individuals have unaffected parents, and all affected cases can trace their ancestry to Samuel King and his wife, who arrived in the area in 1774. It is known that neither King nor his wife was affected with the disorder. There are no cases of the disorder in other Amish communities, such as those in Ohio or Indiana.

What is the most likely explanation for the high frequency of the disorder in the Pennsylvania Amish community and its absence in other Amish communities?