General Genetics spring 2015. Final exam.

Nobody noticed that the final is 90 points rather than 100. That was inadvertent, sorry. So your grades on
this are out of 90, not out of 100.
1. Laying blue-shelled eggs is an autosomal trait in the common chicken. This hen always lays blue eggs.
However, when crossed with a rooster that is known to come from a line true-breeding for white egg shell,
half of her female offspring turned out to be blue egg layers and half white egg layers.
a. (5 pts) Give a genetic explanation of the cross, with illustration.
That was easy. Dominant blue eggs, heterozygous hen. Good illustrations, everybody.
b. (6 pts) OK, so roosters dont lay eggs. Explain how you would determine the genotype of a random male
who is an offspring from this cross. (Explain = demonstrate how it would work)
Test cross was right. It is true that we have always used it to tell between heterozygotes and dominant
homozygotes, but here it also is the only thing you can use, because the white egg laying hen is the only
one whose genotype you know for sure.
2. (10 pts.) Another autosomal gene is responsible for slate-blue feathers which are a very popular
phenotype with breeders. Blue-feathered chicken are called Andalusian. They are not true-breeding
however because they are heterozygotes, a result of codominance. Birds homozygous for one allele are
off-white, and homozygous for the other practically black.
Inheritance of blue-shelled eggs is same as in the previous question.
Both parents are heterozygous for both genes. What is the probability of a hatchling being an Andalusian
blue female who lays blue-shelled eggs? Show your calculations.
Probability of Andalusian blue . Probability of blue eggs = . Probability of being female = .
x x = 3/16.
3. (15 pts.) Two (haploid) strains of the ascomycete Neurospora have been crossed together mutant for
spore color and wild type. The resulting asci were as follows:

count: 16

40
24
a) Calculate the distance between the gene responsible for the spore color and the centromere
(show your calculations);
(16 + 24) x
divide by 80, x 100% = 25 mU
b) Explain the formula you used: how and why is it
- similar to
and
- different from the formula you use when calculating map distances based on testcross results?
Similar because we judge the distance by the % of recombinants important!
Different because we count asci and so on.
Please notice that you cant involve tetratypes here I only have one gene.
And I wouldnt know what anybody meant by parentals and non-parentals because the parents are haploid
wild type and mutant.
c) Imagine that the gene marker is right next to the centromere, no distance at all. In that
case, what would the results be and why? (By results I mean type and # of resulting asci)
No distance no recombination only non-crossover asci - this type.
This kind of problem was explained twice in class and was in the posted test versions. Failures here
indicate no understanding of meiosis, which is quite serious.
4. (15 pts.) The table lists the genotypes of E.coli mutants with changes in the tryptophan operon (the first
line is wild type).
R-O+E+ /FR+ means the genotype of a merozygote with the wild type R gene added on a plasmid vector,
etc. Fill it in.
Phenotype description (transcription
Will the cells be able to survive
inducible, repressible, always repressed, with absolutely no supply of

constitutive?).

tryptophan, y/n?

repressible

repressible

R OE

constitutive

R+OE+/FO+
R-O+E+

constitutive

constitutive

R O E
R O E

RO E
repressible
y
/FR+
I am afraid that the answers showing lack of understand ing of this operon regulation and/ot biological
meaning were graded rather low, regardless of how many answers were randomly guessed correctly..
5. (15 pts.) We discussed how a strain of E. coli was created that produces human insulin.
a) Think about the vector that was used for it. What essential components must it feature?
Polylinker or any convenient sites for cloning, origin of replication, bacterial promoter
b) Is the DNA insert that is cloned into this vector identical to the original human insulin gene? Why or
why not? If the original gene sequence cant be used, what is used in order to express the correct
polypeptide?
cDNA is used because bacterial cells cant do splicing
c) Why do we have to grow two different transformed strains of E. coli in order to produce human
insulin?
(Human insulin is cleaved in two post-translationally and they are rejoined in a certain way to form active
insulin protein. A E. coli cell cant do that, it can only express a polypeptide for us.)
This example was explained carefully in the lecture and shouldnt pose any difficulty to people who were
in attendance.
6. Explain the mechanism of transcription termination in prokaryotes.
Inverted repeat in DNA, hairpin in RNA were all correct. Any replication or translation terminology was
unacceptable here.
7. Explain the mechanism of translation initiation in prokaryotes.
Shine-Dalgarno, 16S ribosome subunit and start codon were all correct. Any replication or transcription
terminology was unacceptable here.
8. In creating modern recombinant versions of eukaryotic genomes, which are the possible approaches to
delivering the genetic information (DNA insert) to the
a. animal cell genome?; Vectors based on retroviruses or even better certain adenoviruses because you
need to use their ability to integrate the insert into chromosomal DNA
b. plant cell genome? Vectors based, however loosely, on the Ti plasmid, for the same reason.
9. What families of viruses include oncogenic viruses and what in their life cycle makes it possible for them
to cause cancer? (Viruses have harmful proteins is not an answer)
Retro (or adeno with an abortive infection cycle!), when a viral protein turns out to be an oncogene.
Extra credit: A historic study by a group of scientists at Caltech dealt with bacteriophage T4 mutants. The
mutants were unable to infect most E. coli cells because of a nonsense mutation in the viral genome
(=resulting in new stop codons - UAG). E. coli strains that allowed the reproduction of those mutant phages
were later called nonsense suppressors.
- What kind of change in the host cell can be a nonsense suppressor, that is to say reverse the effect of
a nonsense mutation in a virus? Explain how it would work.
The first thing that comes to mind is a mutant tRNA in the host, that would recognize the stop codon
for a meaningful one. Thats actually what they found in those suppressors.
Do you expect nonsense suppression to be 100% efficient or fully restore the protein function every
time? Why or why not?
Because the suppressor tRNA is in competition with translation termination factors, the efficiency of
suppression is usually less than 100%, and for other reasons.