1. Describe position effect variegation. What is the structural basis
for this effect and how was it discovered?
2. The following classes and frequencies of ordered tetrads were
obtained from the cross a+ b+ x a b in Neurospora.
______________________________________________________________________________ Spore pair Number of Asci ______________________________________________________________________________ 1-2 3-4 5-6 7-8 a+b+ a+b+ ab ab 1766 a+b+ a b a+b+ ab 220 a+b+ a b+ a+b ab 14
3. The following spore arrangements were obtained in the indicated
frequencies from ordered tetrads in a cross between a Neurospora
straion com/val which exhibits a compact growth form and is unable
to synthesize the amino acid valine, and a wildtype strain +/+.
__________________________________________________________________________________________ Spore pair Ascus composition __________________________________________________________________________________________ 1-2 c v c + c v + v c v 3-4 c v c + c + c + + v 5-6 + + + v + v c v c + 7-8 + + + v + + + + + + Number: 34 36 20 1 9
What can you conclude about the linkage and location of the genes
with respect to each other and to the centromere?
4. The gene met14 in the yeast S. cerevisiae codes for and enzyme used in the synthesis of the amino acid methionine and is very closely linked to the centromere of chromosome XI. Suppose that met14 (m) is used in mapping a new mutation, b, whose location in the genome is unknown. Diploids are made by mating m B x M b, in which the uppercase symbols denote the wildtype alleles, and asci are examined. In this mating, what kinds of asci correspond to parental ditype (PD), nonparental ditype (NPD) and tetratype (TT)? What relative proportions of PD, NPD and TT asci would be expected in the following cases:
5. A gene R codes for a protein that is a negative regulator of transcription of a gene S. Is gene S transcribed in an R- mutation? How does the situation differ if the product of R is a positive regulator of S transcription?
6. For each of the following genotypes, state whether ß-galactosidase is made and whether its synthesis is inducible or constitutive.
7. Let Oo represent an operator mutation causing the operator to bind reversibly with the normal repressor. Let Rs representa a regulatory gene mutation that causes the formation of an altered repressor which cannot react with the inducer even though it can bind with the normal operator. For each of the following, tell which enzymes will be produced constitutively and which by induction?
8. Is it necessary for a gene that codes for the repressor of a bacterial operon to be near the structural genes? Why or why not?
9. Consider a eukaryotic transcriptional activator protein that binds to an enhancer sequence and promotes transcription. What change in regulation would you expect from a duplication in which several copies of the enhancer were present instead of just one?
10. Is an attenuator a region of DNA that, like an operator, binds with a protein? Is RNA synthesis ever initiated at an attenuator?
11. Compare and contrast three structural motifs in eukaryotic transcriptional activator proteins. How do the structures form and how do they facilitate DNA-binding?
12. Draw the essential elements of a eukaryotic promoter. Compare and contrast to prokaryotic promoter regions.
13. In normal mouse cells the protooncogene (p-onc) resides at a certain chromosome site. The DNA in the region of the protooncogene can be broken into specific fragments be a restriction enzyme, as indicated here by the arrows:
____________________________________________________________
p-onc
In the course of an experiment, normal mouse cells growing in culture are
transformed into tumor cells following infection with a retrovirus. You wish
to determine if the malignant transformation is the result of viral integration
near p-onc. DNA is extracted from both normal and transformed cells. The
DNA from both sources is exposed to a restriction enzyme, which fragments
the DNA and attacks the sites indicated previously by arrows. The DNA is
separated according to molecular weight, denatured and exposed to 1)
denatured radioactive p-onc DNA and 2) denatured radioactive viral DNA.
Autoradiographs are then prepared. Interpret teh comparison of the four
autoradiographs shown here:
Cell source of Normal Normal Tumor Tumor
mouse DNA
_______________________________
Molecular weight ______ _____
______
_______________________________
Sources of radiolabeled
DNA: p-onc virus p-onc virus
14. Suppose in the case of another virus, the following results were
obtained in a situation exactly like that described above. What would you
conclude?
Cell source of Normal Normal Tumor Tumor
mouse DNA
_______________________________
Molecular weight ______ _____
______
_______________________________
Sources of radiolabeled
DNA: p-onc virus p-onc virus
15. Progression through the cell cycle depends on the interaction of two
types of regulatory proteins: kinases and cyclins. List the functions of each
and describe how they interact with each other to cause cells to move
through the cell cycle.
16. How were cell cycle checkpoints discovered? How do the checkpoints relate to the cell cycle kinases and cyclins?
17. How would you describe cancer at the cellular level?
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