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Wild-type strains of the haploid fungus Neurospora can make their own tryptophan. An abnormal allele \(t d\) renders the fungus incapable of making its own tryptophan. An individual of genotype \(t d\) grows only when its medium supplies tryptophan. The allele \(s u\) assorts independently of \(t d ;\) its only known effect is to suppress the \(t d\) phenotype. Therefore, strains carrying both \(t d\) and \(s u\) do not require tryptophan for growth. a. If a \(t d ; s u\) strain is crossed with a genotypically wildtype strain, what genotypes are expected in the progeny and in what proportions? b. What will be the ratio of tryptophan-dependent to tryptophan-independent progeny in the cross of part \(a ?\)

Short Answer

Expert verified
The expected genotypes are in a 1:1:1:1 ratio. The ratio of tryptophan-dependent to independent progeny is 1:3.

Step by step solution

01

Understand the Strains

We have two alleles involved: \( td \) which renders the strain tryptophan-dependent unless suppressed and \( su \) which suppresses the \( td \) phenotype leading to tryptophan independence. The wild-type strain produces tryptophan normally, so its genotype is \( td^+ \ su^+ \). In a \( td \ ; su \) strain, both alleles exist: \( td \) is deficient in producing tryptophan while \( su \) negates this deficiency, making the strain tryptophan-independent.
02

Assess the Genotypes in the Cross

Cross \( td \ ; su \) with wild-type \( td^+ \ su^+ \). The possible alleles for \( td \) from one parent are \( td \) and \( td^+ \); for \( su \), the possible alleles are \( su \) and \( su^+ \). Since these alleles assort independently (being on different chromosomes), we expect four types of offspring genotypes, depending on the combination of alleles they receive from each parent.
03

Determine the Genotype Proportions

Use a Punnett Square to determine the possibilities:- Parental Genotypes: \( (td; su) \times (td^+; su^+) \)- Possible Gametes from \( td; su \): \( td \ su \) - Possible Gametes from \( td^+; su^+ \): \( td^+ \ su^+ \)The resulting progeny genotypes, assuming independence, are:1. \( td^+ \ su^+ \) (wild-type)2. \( td^+ \ su \) 3. \( td \ su^+ \)4. \( td \ su \)As these are independent alleles, the genotypes will appear in equal proportions: 1:1:1:1.
04

Evaluate Phenotypic Expressions

Only the genotype \( td \ su \) will result in tryptophan independence since \( su \) suppresses the \( td \) phenotype. The other genotypes \( td^+ \ su^+ \), \( td^+ \ su \), and \( td \ su^+ \) will show either the wild-type ability to synthesize tryptophan or continue to be tryptophan-dependent.
05

Calculate Tryptophan Dependence Ratio

Of the genotypes, only \( td \ su \) results in tryptophan independence. The other genotypes \( td^+ \ su^+ \) and \( td^+ \ su \) are also independent due to the presence of \( td^+ \). Only \( td \ su^+ \) remains tryptophan-dependent. Since \( td \ su^+ \) appears once in the possible outcomes (out of four), we have a 1:3 ratio for tryptophan-dependent to independent progeny.

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Key Concepts

These are the key concepts you need to understand to accurately answer the question.

Neurospora genetics
Neurospora, a type of haploid fungus, serves as a model organism for genetic studies. Haploidy means that each cell contains only one set of chromosomes. This characteristic simplifies genetic analysis, as the effects of mutations become immediately apparent. Neurospora genetics offers insights into genetic inheritance and variation. In this context, an allele is a variant form of a gene. Alleles can influence traits such as a strain's ability to produce tryptophan, an essential amino acid. Understanding neurospora genetics involves understanding how alleles interact. For instance, in the exercise, the allele "td" causes a deficiency in tryptophan production unless it's suppressed by another allele called "su." Scientists study these interactions by crossing different genetic strains and observing how traits, such as tryptophan dependence, are inherited in the progeny.
tryptophan biosynthesis
Tryptophan is one of the essential amino acids that organisms, including fungi like Neurospora, need to synthesize for survival. Tryptophan biosynthesis is a complex biochemical pathway involving multiple enzymes that transform precursor molecules into tryptophan. Typically, wild-type strains of Neurospora can produce tryptophan naturally without external sources. However, certain mutations, such as "td," disrupt this pathway, leading to a strain incapable of synthesizing its own tryptophan. This "td" mutation means the organism has to rely on external sources for this amino acid unless the defect is counteracted by another mutation. In our exercise example, the allele "su" can suppress the effects of "td," restoring tryptophan independence without directly contributing to the biosynthesis pathway itself.
allele suppression
Allele suppression is a fascinating genetic phenomenon where the effect of one allele (mutation) is negated or suppressed by another. In the case of Neurospora, the suppressor allele "su" counteracts the impact of "td," which would typically prevent tryptophan production. When suppression occurs, the presence of the "su" allele modifies the expected biochemical or phenotypic expression of the underlying mutant pathway, effectively "neutralizing" the defect. This suppression enables the organism to function as if the original mutation ("td") does not exist, highlighting the complexity and adaptability of genetic pathways. Understanding allele suppression is crucial in genetic studies as it can provide insights into gene interactions and regulatory mechanisms.

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Most popular questions from this chapter

Because snapdragons (Antirrhinum) possess the pigment anthocyanin, they have reddish purple petals. Two pure anthocyaninless lines of Antirrhinum were developed, one in California and one in Holland. They looked identical in having no red pigment at all, manifested as white (albino) flowers. However, when petals from the two lines were ground up together in buffer in the same test tube, the solution, which appeared colorless at first, gradually turned red. a. What control experiments should an investigator conduct before proceeding with further analysis? b. What could account for the production of the red color in the test tube? c. According to your explanation for part \(b\), what would be the genotypes of the two lines? d. If the two white lines were crossed, what would you predict the phenotypes of the \(\mathrm{F}_{1}\) and \(\mathrm{F}_{2}\) to be?

In one species of Drosophila, the wings are normally round in shape, but you have obtained two pure lines, one of which has oval wings and the other sickle-shaped wings. Crosses between pure lines reveal the following results: $$\begin{array}{llll} {3}{c} {\text {Parents}} & {2}{c} {F 1} \\ \hline \text { Female } & \text { Male } & \text { Female } & \text { Male } \\\ \hline \text { sickle } & \text { round } & \text { sickle } & \text { sickle } \\ \text { round } & \text { sickle } & \text { sickle } & \text { round } \\ \text { sickle } & \text { oval } & \text { oval } & \text { sickle } \\ \hline \end{array}$$ a. Provide a genetic explanation of these results, defining all allele symbols. b. If the \(F_{1}\) oval females from cross 3 are crossed with the \(\mathrm{F}_{1}\) round males from cross \(2,\) what phenotypic proportions are expected for each sex in the progeny?

In the nematode \(C .\) elegans, some worms have blistered cuticles due to a recessive mutation in one of the bli genes. Someone studying a suppressor mutation that suppressed bli-3 mutations wanted to know if it would also suppress mutations in \(b l i-4 .\) They had a strain that was homozygous for this recessive suppressor mutation, and its phenotype was wild type. a. How would they determine whether this recessive suppressor mutation would suppress mutations in bli- 4 ? In other words, what is the genotype of the worms required to answer the question? b. What cross(es) would they do to make these worms? c. What results would they expect in the \(\mathrm{F}_{2}\) if (1) it did act as a suppressor of bli-4? (2) it did not act as a suppressor of bli- 4 ?

Consider two blood polymorphisms that humans have in addition to the ABO system. Two alleles \(L^{\mathrm{M}}\) and \(L^{\mathrm{N}}\) deter mine the \(\mathrm{M}, \mathrm{N},\) and \(\mathrm{MN}\) blood groups. The dominant allele \(R\) of a different gene causes a person to have the \(\mathrm{Rh}^{+}\) (rhesus positive) phenotype, whereas the homozygote for \(r\) is \(\mathrm{Rh}^{-}(\text {rhesus negative }) .\) Two men took a paternity dispute to court, each claiming three children to be his own. The blood groups of the men, the children, and their mother were as follows: $$\begin{array}{llll} \text { Person } & {3}{c} {\text { Blood group }} \\ \hline \text { husband } & \mathrm{O} & \mathrm{M} & \mathrm{Rh}^{+} \\ \text {wife's lover } & \mathrm{AB} & \mathrm{MN} & \mathrm{Rh}^{-} \\ \text {wife } & \mathrm{A} & \mathrm{N} & \mathrm{Rh}^{+} \\ \text {child 1 } & \mathrm{O} & \mathrm{MN} & \mathrm{Rh}^{+} \\ \text {child 2 } & \mathrm{A} & \mathrm{N} & \mathrm{Rh}^{+} \\ \text {child 3 } & \mathrm{A} & \mathrm{MN} & \mathrm{Rh}^{-} \\ \hline \end{array}$$ From this evidence, can the paternity of the children be established?

If a man of blood-group AB marries a woman of bloodgroup A whose father was of blood-group \(\mathrm{O}\), to what different blood groups can this man and woman expect their children to belong?

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