- Compare Figure 7.3.1 and Table 7.3.1 in Section 7.3 Suppose you created three new arg– mutation called mutants #1, #2, & #3. #1 grew on MM+cit and MM+arg, #2 grew on only MM+arg, while #3 grew on MM+ orn, cit or arg. Which genes are #1, 2, & 3 mutant in (A, B, or C)?
- Why was the Vitamin biotin always added the MM?
- Last century, A. Garrod, and later Beadle and Tatum, showed that genes encode enzymes. From what we know now, do all genes encode enzymes? Explain.
- Most mutant proteins differ from wild type (normal) by a single substitution at a specific amino acid site. Explain how some amino acid changes result in:
- no loss of protein function,
- only partial loss-of-function,
- complete loss-of-function,
- and how do changes at different amino acid sites result in the same complete loss-of-function.
- Some mutants result in the loss of a specific enzyme activity. Does this mean that no protein product is produced from that mutant gene?
- The molecular weight of the A and B chains of coli tryptophan synthase are 29,500 and 49,500, respectively. The size of the entire enzyme is 158,000.
- If the average molecular weight of each amino acid is 110, then how many amino acids are present in each chain?
- How many chains does the whole enzyme contain? Explain.
- Recall that Neurospora is orange coloured bread mould. This biochemical pathway below is how wild type cells become orange. None of the compounds are essential. Cells containing W are white, cells with Y are yellow, and cells with O are orange. Assume that the reactions will go to completion, if possible.Fill in this table with the colours of the cell cultures.
Strain MM+W MM+Y MM+O gene1+
- You have a female fruit fly, whose father was exposed to a mutagen (she, herself, wasn’t). Mating this female fly with another non-mutagenized, wild-type male produces offspring that all appear to be completely normal, except there are twice as many daughters as sons in the F1 progeny of this cross.
- Propose a hypothesis to explain these observations.
- How could you test your hypothesis?
- You decide to use genetics to investigate how your favourite plant makes its flowers smell good.
- What steps will you take to identify some genes that are required for production of the sweet floral scent? Assume that this plant is a self-pollinating diploid.
- One of the recessive mutants you identified has fishy-smelling flowers, so you name the mutant (and the mutated gene) fishy. What do you hypothesize about the normal function of the wild-type fishy gene?
- Another recessive mutant lacks floral scent altogether, so you call it nosmell. What could you hypothesize about the normal function of this gene?
- Suppose you are only interested in finding dominant mutations that affect floral scent.
- What do you expect to be the relative frequency of dominant mutations, as compared to recessive mutations, and why?
- How will you design your screen differently than in the previous question, in order to detect dominant mutations specifically?
- Which kind of mutagen is most likely to produce dominant mutations, a mutagen that produces point mutations, or a mutagen that produces large deletions?
- You are interested in finding genes involved in synthesis of proline (Pro), an amino acid that is normally synthesizes by a particular model organism.
- How would you design a mutant screen to identify genes required for Pro synthesis?
- Imagine that your screen identified ten mutants (#1 through #10) that grew poorly unless supplemented with Pro. How could you determine the number of different genes represented by these mutants?
- If each of the four mutants represents a different gene, what will be the phenotype of the F1 progeny if any pair of the four mutants are crossed?
- If each of the four mutants represents the same gene, what will be the phenotype of the F1 progeny if any pair of the four mutants are crossed?