Becker's World of the Cell (9th Edition)
9th Edition
ISBN: 9780321934925
Author: Jeff Hardin, Gregory Paul Bertoni
Publisher: PEARSON
expand_more
expand_more
format_list_bulleted
Concept explainers
Videos
Textbook Question
Chapter 17, Problem 17.10PS
Mutatis mutandis You work in a lab that uses the nematode C. elegans as a model organism. You find that one of the strains you are using has an inexplicably high incidence of mutations. It turns out this is because this strain is carrying an active transposon that was accidentally introduced into the strain. Indeed, such strains are called “mutator” strains by labs that work on worms. Why would a transposon cause such a high incidence of mutation?
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solution
Students have asked these similar questions
Materials
In order to determine the genetic material of a T2 phage, Alfred Hershey and
Martha Chase conducted experiments using T2 phages that infected bacteria. In
one treatment, they grew phages with radioactive sulfur. In another treatment,
they grew phages with radioactive phosphorous. They allowed both types of
phages to infect bacterial cells. After infection, they found that only bacteria
infected with phages grown with radioactive phosphorous showed any
radioactivity. Why did they use radioactive sulfur and phosphorous for this
Updates
Grades
Members
O Conferences
DBQ Online
experiment? *
Newsela
ormation
O Sulfur is part of the DNA molecule but not part of a protein molecule.
Biology Periods 1 and 2
Sulfur and phosphorous are some of the most reactive molecules and are easily
ding periods
school MP1, Highschool
Highschool MP3,
school MP4
traced.
Sulfur and phosphorous are able to survive the centrifuge, a crucial component of the
experiment.
ion
Phosphorous is part of the DNA…
The genetic alteration responsible for sickle-cell anemia in humans involves:
a transition mutation from A to G, substituting glutamic acid for valine in a-globin
a transversion mutation from T to A, substituting valine for glutamic acid in b-globin
a transition mutation from T to C, substituting valine for glutamic acid in b-globin
a transversion mutation from G to C, substituting glutamic acid for valine in a-globin
a frameshift mutation of one ATC codon, removing glutamic acid from b-globin
Most organisms display a circadian rhythm, a cycling of biological processes that is roughly synchronized with day length. In Drosophila, pupae eclose (emerge as adults after metamorphosis) at dawn.
a)Using this knowledge how would screen for Drosophila mutants that have an impaired circadian rhythm?
b)In each case, how would you clone the genes you identified by mutation?
Chapter 17 Solutions
Becker's World of the Cell (9th Edition)
Ch. 17 - The theoretical amplification accomplished by n...Ch. 17 - Bacterial replication and that in typical...Ch. 17 - Nonhomologous end-joining and synthesis-dependent...Ch. 17 - Prob. 17.3CCCh. 17 - Meselson and Stahl Revisited. For each of the...Ch. 17 - DNA Replication. Sketch a replication fork of...Ch. 17 - More DNA Replication. The following are...Ch. 17 - QUANTITATIVE Still More DNA Replication. Suppose...Ch. 17 - The Minimal Chromosome. To enable it to be...Ch. 17 - Prob. 17.6PS
Knowledge Booster
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- Consider three genes in E. coli: thr+, ara+, and leu+ (which give the cell the ability to synthesize threonine, arabinose, and leucine, respectively). All three of these genes are close together on the E. coli chromosome. Phages are grown in a thr+ ara+ leu+ strain of bacteria (the donor strain). The phage lysate is collected and used to infect a strain of bacteria that is thr− ara− leu −. The recipient bacteria are then tested on selective medium lacking leucine. Bacteria that grow and form colonies on this medium (leu+ transductants) are then replica-plated on medium lacking threonine and on medium lacking arabinose to see which are thr+ and which are ara+. Another group of the recipient bacteria are tested on medium lackingthreonine. Bacteria that grow and form colonies on this medium (thr+ transductants) are then replica-plated on medium lacking leucine and onto medium lacking arabinose to see which are ara+ and which are leu+. Results from these experiments are as follows:…arrow_forwardTermicin is a small antifungal protein in termites that is produced by cells and secreted into termite saliva in response to a pathogen. In vitro translation of the termicin-encoding gene is performed, and the effects of that product are compared to those of termicin extracted from a termite. You see that extracted termicin exhibits more antifungal behavior than in vitro translated termicin. After further analysis, you see that extracted termicin contains 3 disulfide bonds, while in vitro translated termicin contains zero. The addition of microsomes to the in vitro translation reaction results in termicin with all 3 disulfide bonds. What experimental condition is most likely responsible for this difference? A. in vitro translation was not performed at the correct temperature affecting protein folding B. a mutation occurred during in vitro translation, leading to differences in disulfide bond formation O C. the UPR can not be activated in vitro, therefore, this protein can only be…arrow_forwardLet’s suppose you make a transposon library of the cellulose-secreting bacterium Komagataeibacter xylinus, with the goal of finding mutants that produce higher than normal amounts of cellulose, which would be useful industrially. However, despite your best efforts you are unable to isolate any transposon mutants that make more cellulose than the wild-type strain.Why might this have failed? List as many reasons as you can think of.arrow_forward
- Inhibitors for this reverse transcriptase fall in two classes: nucleoside analog inhibitors (NRTIs) or non-nucleoside analog inhibitors (NNRTIs). NRTIs have a similar structure to nucleosides and block the active site of the reverse transcriptase, whereas NNRTIs don't look like nucleosides and bind to an allosteric pocket in the reverse transcriptase. Presently NNRTIs are used more often than NRTIs, as NRTIs have more severe side effects. Why do you think NRTIs would have severe side effects?arrow_forwardWhich of the following is not an example of a transversion mutation? a) T·A -> C·G b) G·C -> C·G c) T·A -> G·C d) C·G -> A·T e) A·T -> T·Aarrow_forwardA research group is studying a bacterium X that binds to mucosal cells in the lung and invades. Wildtype X has an LD50 value of 10 bacteria when administered to mice by inhalation. Using transposon mutagenesis, the researchers have isolated two mutants of X that they call Xmut1 and Xmut2, both of which have LD50 values of 105 when inhaled by mice. However, in tissue culture cells, Xmut1 can invade the cells just as well as wild-type X, while Xmut2 cannot. Provide a possible explanation for these results.arrow_forward
- In a study, bacterial culture of E. coli was infected with bacteriophage. How- ever, these cultures were protected from phage infection. Interestingly, it was found that the resistance is due to endonudeases present in E. coli, which deaved the phage DNA. How is the E. coli genomic DNA protected from the action of these endonuclease enzymes?arrow_forwardThe genes for both the α- and βglobin chains of hemoglobin contain introns (i.e., they are split genes). How would this fact affect your plans if you wanted to introduce the gene for α-globin into a bacterial plasmid and have the bacteria produce α-globin?arrow_forwardA gene contains the sequence CGCATACGGTAC that results in the amino acid sequence arg-ile-arg- tyr. A mutation in this gene has a G inserted after the second C in the strand. How will this mutation affect the phenotype? A:This will affect the phenotype because although most of the protein will be identical, the first amino acid will be different. B:This will not affect the phenotype because only the second amino acid is different from the original protein. C:This will not affect the phenotype because the protein will be identical to the original protein. D:This will affect the phenotvpe because all of the amino acids after the first one will be different from he original protein.arrow_forward
- A newly identified protein from the cells of the Panopyra plant on Pandora was shown to inhibit translation of its target genes by binding to the 5’ UTR of the mRNA and preventing ribosome binding. A possible way this inhibition may be relieved by an sRNA would be: Group of answer choices a)The sRNA acts as a silencer, suppressing the inhibitory protein and allowing translation to take place. b)The sRNA acts as a decoy, sequestering the inhibitory protein and allowing translation to take place. c)The sRNA acts as a marker, flagging the inhibitory protein for ubiquitination and allowing translation to take place.arrow_forwardThe amino acid asparagine is synthesized from aspartic acid by the enzyme asparagine synthetase (AS). In the previous problem you proposed a model for how this gene could be regulated. Suppose that you carry out an experiment to test your model. To do this you cut out the regulatory sequences upstream of the gene and fuse it to a gene for green fluorescent protein (GFP). Now you can visually observe when the gene is activated. You insert this engineered gene into a host cell and look for GFP expression. You discover some mutants that have different expression levels of GFP and call them GFP1- and GFP2-. The expression levels of GFP are given below. Cell GFP expression Wild type 100 GFP1- 50 GFP2- 0 Propose an explanation for these results based on your model. In other words, what was mutated and how? Your answer should include whether the mutation is (see links for more information): dominant or recessive https://www.ncbi.nlm.nih.gov/books/NBK21578/#A1877…arrow_forwardThe amino acid asparagine is synthesized from aspartic acid by the enzyme asparagine synthetase (AS). In the previous problem you proposed a model for how this gene could be regulated. Suppose that you carry out an experiment to test your model. To do this you cut out the regulatory sequences upstream of the gene and fuse it to a gene for green fluorescent protein (GFP). Now you can visually observe when the gene is activated. You insert this engineered gene into a host cell and look for GFP expression. You discover some mutants that have different expression levels of GFP and call them GFP1- and GFP2-. The expression levels of GFP are given below. Cell GFP expression Wild type 100 GFP1- 50 GFP2- 0 Propose an explanation for these results based on your model. In other words, what was mutated and how? This answer should include whether the mutation is (view links for more information): dominant or recessive https://www.ncbi.nlm.nih.gov/books/NBK21578/#A1877 in a cis…arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
Human Anatomy & Physiology (11th Edition)BiologyISBN:9780134580999Author:Elaine N. Marieb, Katja N. HoehnPublisher:PEARSON
Biology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStax
Anatomy & PhysiologyBiologyISBN:9781259398629Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa StouterPublisher:Mcgraw Hill Education,
Molecular Biology of the Cell (Sixth Edition)BiologyISBN:9780815344322Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter WalterPublisher:W. W. Norton & Company
Laboratory Manual For Human Anatomy & PhysiologyBiologyISBN:9781260159363Author:Martin, Terry R., Prentice-craver, CynthiaPublisher:McGraw-Hill Publishing Co.
Inquiry Into Life (16th Edition)BiologyISBN:9781260231700Author:Sylvia S. Mader, Michael WindelspechtPublisher:McGraw Hill Education
Human Anatomy & Physiology (11th Edition)
Biology
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:PEARSON
Biology 2e
Biology
ISBN:9781947172517
Author:Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher:OpenStax
Anatomy & Physiology
Biology
ISBN:9781259398629
Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa Stouter
Publisher:Mcgraw Hill Education,
Molecular Biology of the Cell (Sixth Edition)
Biology
ISBN:9780815344322
Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter
Publisher:W. W. Norton & Company
Laboratory Manual For Human Anatomy & Physiology
Biology
ISBN:9781260159363
Author:Martin, Terry R., Prentice-craver, Cynthia
Publisher:McGraw-Hill Publishing Co.
Inquiry Into Life (16th Edition)
Biology
ISBN:9781260231700
Author:Sylvia S. Mader, Michael Windelspecht
Publisher:McGraw Hill Education
QCE Biology: Introduction to Gene Expression; Author: Atomi;https://www.youtube.com/watch?v=a7hydUtCIJk;License: Standard YouTube License, CC-BY