Genetics 371B Practice problems--Autumn 2000 week 9

Lectures 27-29

1. For each partially diploid E. coli strain shown below, indicate whether beta-galactosidase activity will be inducible, non-inducible (i.e., low in the presence or absence of inducer), or constitutive. Give a one-sentence explanation for each answer.
(a)
i+ p+ oc z+
i- p+ o+ z-
(b)
is p+ o+ z+
i+ p+ o+ z+
(c)
i- p- oc z+
i+ p+ oc z-
(d)
is p- o+ z+
i- p- oc z+
(e)
i- p- o+ z+
i+ p+ o+ z-
As discussed in class, i- mutations prevent binding of repressor to the operator; is mutations result in "super-repressors" that cannot be dislodged from the promoter, p- mutations prevent transcription initiation from the promoter, oc mutations prevent binding of repressor to the operator, and z- mutations cause production of non-functional beta-galactosidase.

2.

Homework question from 1998

Buffy is curious about the genetics of vampirism. As luck would have it, she is at a rave in the wilds of East Olympia when she notices a fruit fly trying to bite her on the neck. Hoping that she has discovered a vampire variety of Drosophila , she captures a few of the bloodthirsty creatures and brings them back to her lab in Kent. Sure enough, the "fruit" flies show many of the classic symptoms of vampirism: in response to the smell of blood, they grow little fangs and try to bite people (and other flies) on the neck, and this response is completely blocked by the odor of garlic. Further investigation reveals that the vampire response requires transcription of a gene that Buffy calls the Vamp gene, and that this response is regulated by two other protein-coding genes, B and G:

    Genotype Condition Vamp mRNA level
    Wildtype no blood, no garlic low
    Wildtype blood, no garlic high
    Wildtype blood + garlic low
    B-/B- no blood, no garlic high
    B-/B- garlic low
    G-/G- any low
    B+/B- no blood, no garlic low
    G+/G- blood, no garlic high
    B-/B- G-/G- any low

Propose a model for the regulation of Vamp gene transcription. Briefly explain how you arrived at your model.

3. Modified exam question from 1998

Superchickens on the planet Krypton are as powerful as locomotives. Their exact power can be assayed be seeing how many locomotives they can stop. However, superchickens are sensitive to kryptonite -- when exposed to kryptonite, they cannot even stop a Ballard pedestrian, let alone locomotives. You have identified a dominant mutation that confers resistance to kryptonite. It turns out that this dominant mutation is in loco, a protein-coding gene, and that the defect results in failure to regulate transcription of the krypto gene correctly. (The krypto gene coding region is itself normal; it's the regulation that is abnormal.)

(a)
Suggest two alternative models for the role of the normal loco gene, explaining in one sentence the phenotype of the mutant in each case. Assume for both models that krypto gene transcription is required for locomotive-stopping power.
(b) Saturation mutagenesis turns up only more alleles of loco, suggesting that krypto transcription is regulated solely by loco; no other genes are involved. Assuming that this conclusion is valid, which of your two models can you now rule out, and why?
(c) Why might the assumption in part (b) be a bad assumption to make?

4. Diagram a series of crosses that would allow you to screen for maternal effect mutations in Drosophila.

5. In a Drosophila embryo homozygous for a bicoid null allele, what do you predict about the expression pattern of hunchback protein? What about in an embryo overexpressing bicoid? What about bicoid expression in a hunchback mutant embryo?

6. Many maternal effect genes are hard to study because they also have non-maternal roles later in development. (Why would that make them hard to study?) Assuming you have a dominant female sterile marker gene you can put anywhere in the genome, and a potent source of X-rays, suggest two strategies that would let you study the maternal role of a gene located halfway along the second chromosome of Drosophila.