MBG 3080 Study Guide - Cole1, Lac Operon, Repressor Lexa

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fuchsiaporpoise864

2 Dec 2013

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University of Guelph

Department

Molecular Biology and Genetics

Course

MBG 3080

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Document Summary

Sample questions for mt-2, fall/2012: describe the role of the following components in cole1 biology, you have been given a strain of e. coli carrying a mutation in the lexa gene. How will this strain survive uv irradiation compared to the wild type strain: a lacz- mutant was recovered at a frequency of approximately 10-4. The mutant also acquired resistance to ampicillin simultaneously. You suspected that it might have been caused by the integration of a tn3 into the lacz gene. You have obtained the nucleotide sequence of the mutated lacz gene for comparison with the wild-type lacz sequence. Describe three characteristics of the sequences that support the hypothesis of tn3 insertion into the lacz gene: a tetr plasmid carries a temperature sensitive mutation in its origin of replication and cannot replicate at 42oc. This plasmid was introduced into tets e. coli cells to produce.

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Flies with a dominant mutation in a particular gene have an additional set of wings. Through mapping techniques, you identify a candidate gene, gene X, on an autosomal chromosome that you think results in extra wings when mutated. When you sequence gene X in the mutant fly with extra wings, you notice a missense mutation in the middle of the coding region of gene X. What is the best way to verify that the mutation in gene X is responsible for the dominant phenotype?

a. Starting with a wild-type fly, knockout gene X to generate a null allele and see if flies that are heterozygous or homozygous for the null allele have extra wings.

b. Starting with the mutant fly that is heterozygous for the dominant allele, insert a wild type copy of gene X (complete with its own promoter) elsewhere in the genome of the fly and see if it rescues the mutant and results in normal/wild-type wings.

c. Starting with a mutant fly that is heterozygous for the dominant allele, replace the dominant mutant allele with a wild type version of the gene via homologous recombination and see whether flies with the replacement have normal/wild type wings.

d. Starting with a homozygous wild-type fly, replace one copy of wild-type gene X with a version carrying the dominant mutation via homologous recombination, and see whether flies with the replacement have extra wings.

e. either C or D

You have a strain of flies that are homozygous for a deletion of 2 neighboring genes, A and B (genotype aabb). Wild type flies have transparent wings but these aabb flies have rainbow-colored wings. Which of the following experiments would provide you with more information about which of these genes (if either) is responsible for the rainbow-colored wings?

a. Starting with a wild-type fly, create a transgenic fly that is homozygous for deletion in both genes A and B and see if you get the rainbow-colored wings.

b. Delete gene A alone and gene B alone in 2 independent wild-type flies and see whether flies homozygous for either deletion have rainbow-colored wings.

c. Starting with a mutant fly with rainbow-colored wings, introduce both wildtype genes A and B into a new place in the genome of the fly and see if normal wing color is restored.

d. non of the above

please answer all the questions answering only one question is not helpful!
Question 1

0 / 1 pts

Which of the following E. coli strains with the lac genotypes will synthesize beta-galactosidase in the presence of lactose?

Note: Superscript wouldn't work in the answers, so for example, lacIs means lacI^s(superrepressor of lacI)

lacIâ lacPâ lacOâ lacZâ lacYâ

lacIs lacP+ lacO+ lacZ+ lacYâ / lacI+ lacP+ lacO+ lacZâ lacY+

lacIs lacPâ lacO+ lacZâ lacY+ / lacI+ lacP+ lacO+ lacZ+ lacY+

lacIâ lacPâ lacO+ lacZ+ lacY+

lacI+ lacP+ lacO+ lacZ+ lacY+

Question 2

0 / 1 pts

Some mutations in the trp 5' UTR region increase termination by the attenuator. An example of a mutation that may have this effect is a

Choose the best answer!

mutation that changes the bases in region 3 of the 5' UTR, such that they no longer pair with region 2 or 4.

deletion of the two tryptophan codons in the 5' UTR leader peptide.

deletion in region 2 in the 5' UTR that prevents it from pairing with region 3.

The second and third answers are correct.

The first, second, and third answers are correct.

IncorrectQuestion 3

0 / 1 pts

Several examples of antisense RNA regulating translation in bacterial cells have been discovered. If you wanted to design a construct to artificially control translation of a bacterial gene with antisense RNA, what type of sequences should the antisense RNA contain?

A sequence complementary to the operator of an operon.

A sequence complementary to a 5' UTR.

A sequence complementary to the Shine-Dalgarno site of the mRNA.

The first and second choices are correct.

The second and third choices are correct.

Question 4

0 / 1 pts

Which of the following correctly describes the function of microRNAs?

Choose the best answer.

MicroRNAs are encoded by genes in the genome of an organism.

MicroRNAs form mRNA which encodes a protein repressor for another gene.

MicroRNAs encode a mRNA that base pairs with itself, forming double stranded RNA.

MicroRNAs are cut into small pieces, then bound by the complex of proteins called RISC to repress the translation of other mRNAs in the cell.

The first and second answers are correct.

The first, third, and fourth answers are correct.

The third and fourth answers are correct.

whitemole409

In a genetic experiment:

The use and limits of RNA interference as a reverse genetics technique for knocking down gene expression were tested. The wild-type and mutants worms for the strains were selected. The RNAi feeding strains and control bacterial were used for the the RNAi experiment. The eri-1 C. elegan strains (wild-type) were used for RNAi treatment and mutant strains that were used ( unc-22 and dpy-13) C. elegans. Both carbencillin and IPTG wered added to the RNAi feeding plates and E.coli containing the RNAi transgenes were spread on the plates. The antibodic carbacillin only allows growth of bacteria which contains the RNAI construct. IPTG induces the expression of the polymerase which then transcribes the siRNA in the bacteria. 6 NGM plates without bacteria were used and 20ul of 12.5 mg/ml carbencillin concentration were spread on the 6 of the plates. The carbencillin dried and then IPTG was spread (25ug/ml) on each plate. Then 6 plates with the RNAi bacterial strains were used. Theree of plates for strain one and the other three for strain the second strain. When IPTG dried , 150 ul of the appropraite bacteria was added onto each plate. 2NGM plates (without carbenicillin or IPTG) was spread with 150 ul of OP50 bacterial culture. OP50 is the regular E. coli strain for culturing C. elegans and does not contain the RNAi constructs. These plate were used as the control plates6. Then the plates were incubated for two days. Then the adult hermaphrodites from the RNAi feeding plates and the op50 plates were removed. Then from the eri-1 wildtype stock, 2 or 3 L4 hermaphrodites or
young adults were transferred onto each RNAi feeding plate. Then L4 worms were transferred to an intermediate plate first. After they have a minute to move away from each other and the eggs, and transfered to the RNAi plates. On the two control plates seeded with OP50, 2 L4 or young adult hermaphrodites were placed there. Plates were obtain as the reference mutants (unc-22, bli-1 or unc-13). Then the plates were incubated to allow the worm to develop and lay eggs in two days. Then the adult hermaphrodites from your RNAi feeding plates and the op50 plates were removed and then placed back into the incubator.

The op500 was the negative control plate wtih 80 and 300 progeny and unc-22 had around 50. (reference plates)

Mating in the RNAi plates

Dpy (60) x wildtype (15) and unc( 70) x wildtype ( 8) progeny

the phenotype was movement and it seemed similar phenotype within the progeny.

Can you help me understand the results and what is happening genetically in the experiment ? Are the for dyp-15 x unc-22 mating cross and unc-22 x eri-1 wildtype C. elegans. Based on the data:

Briefly discuss the results of the RNAi experiment. How closely did the RNAi-treated worms phenocopy the mutant worms?

Was the gene knockdown 100% effective?

Was the RNAi treatmentequally effective for the two genes? If not, discuss this result and why that could occured.

Please be specific and detailed

Genetics HELP ASAP

MBG 3080 Study Guide - Cole1, Lac Operon, Repressor Lexa

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