Genetics: From Genes to Genomes
6th Edition
ISBN: 9781259700903
Author: Leland Hartwell Dr., Michael L. Goldberg Professor Dr., Janice Fischer, Leroy Hood Dr.
Publisher: McGraw-Hill Education
expand_more
expand_more
format_list_bulleted
Concept explainers
Textbook Question
Chapter 15, Problem 19P
A mutant haploid strain of Saccharomyces cerevisiae (yeast) called cox2-1 was found that was unable to grow on media containing glycerol as the sole source of carbon and energy. (Glycerol is a nonfermentable substrate for yeast.) This strain could, however, grow on the fermentable substrate glucose. Researchers discovered that cox2-1 cells lack a mitochondrial protein called cytochrome c oxidase.
a. | Explain why cox2-1 cells can grow on medium containing glucose but not on glycerol medium. |
b. | When cox2-1 was crossed with a wild-type yeast strain and the resultant diploid cells were allowed to grow mitotically, it was found that about half the diploid clones were able to grow on glycerol, while the other half could not. The diploid clones that could grow on glycerol were induced to sporulate, and they yielded tetrads with four spores that were all able to grow on glycerol medium. In all of these tetrads, two of the haploid progeny were of mating type a and two of mating type α. The diploids that could not grow on glycerol could not sporulate. What do the results of the mating say about the location of the cox2-1 mutation? |
c. | A different mutant strain of yeast called pet111-1 is also unable to grow on glycerol medium but still can grow on glucose medium. These mutant cells similarly lacked the cytochrome c oxidase. When pet111-1 was crossed with a wild-type haploid strain of the opposite mating type, the resultant diploids were able to grow on glycerol and yielded asci that all showed a 2:2 segregation of haploid cells that could or could not grow on glycerol. Explain these results in light of your answer to part (b) |
Expert Solution & Answer
Trending nowThis is a popular solution!
Students have asked these similar questions
A mutant haploid strain of Saccharomyces cerevisiae(yeast) called cox2-1 was found that was unable togrow on media containing glycerol as the sole sourceof carbon and energy. (Glycerol is a nonfermentablesubstrate for yeast.) This strain could, however, growon the fermentable substrate glucose. Researchers discovered that cox2-1 cells lack a mitochondrial proteincalled cytochrome c oxidase.a. Explain why cox2-1 cells can grow on mediumcontaining glucose but not on glycerol medium.b. When cox2-1 was crossed with a wild-type yeaststrain and the resultant diploid cells were allowedto grow mitotically, it was found that about half thediploid clones were able to grow on glycerol, whilethe other half could not. The diploid clones thatcould grow on glycerol were induced to sporulate,and they yielded tetrads with four spores that wereall able to grow on glycerol medium. In all of thesetetrads, two of the haploid progeny were of matingtype a and two of mating type α. The diploids thatcould not…
In early studies of cultured cells, a respi-
ration-deficient mutant of Chinese hamster
fibroblasts was found. The respiration rate
of the mutant cell line was only 8% of the
wild type cell line. It was determined that
that all enzymes of the Krebs cycle or Tri-
carboxylic Acid Cycle were present in the
mutant. Also, absorption spectra of the cy-
tochrome content of mitochondria showed
no deficit in cytochrome content. Various
assays were carried out and results are il-
lustrated below.
moles 02 consumed / hr/mg protein
2.0)
15
0.5
A
Succinate a-glycerol-
phosphate
0.4
0.3
0.2
01
4.
B
Malate Glutamate d-Keto- Isocitrate
glutarate
(a)
Rates of reduction of O2 catalyzed by wild type and mutant mitochondria and supported by
oxidation of substrates are compared by the histogram graph on the previous page. Open bars rep-
resent Wild Type mitochondria; cross-hatched bars represent the mutant mitochondria. Oxidation of
each of the substrates in the two graphs requires a coenzyme. On what…
A mutant haploid strain of Saccharomyces cerevisiae(yeast) called cox2-1 was found that was unable togrow on media containing glycerol as the sole sourceof carbon and energy. (Glycerol is a nonfermentablesubstrate for yeast.) This strain could, however, growon the fermentable substrate glucose. Researchers discovered that cox2-1 cells lack a mitochondrial proteincalled cytochrome c oxidase.a. Explain why cox2-1 cells can grow on mediumcontaining glucose but not on glycerol medium.
Chapter 15 Solutions
Genetics: From Genes to Genomes
Ch. 15 - Match each numbered item with the most closely...Ch. 15 - Assuming human cells have on average 1000...Ch. 15 - Reverse translation is a term given to the process...Ch. 15 - The human nuclear genome encodes tRNAs with 32...Ch. 15 - The human mitochondrial genome includes no genes...Ch. 15 - How do you know if the halibut you purchased at...Ch. 15 - Is each of these statements true of chloroplast or...Ch. 15 - Suppose you are characterizing the DNA of a...Ch. 15 - An example of a gene-targeting DNA plasmid vector...Ch. 15 - Which of the following characteristics of...
Ch. 15 - The Saccharomyces cerevisiae nuclear gene ARG8...Ch. 15 - The so-called hypervariable regions HV1 and HV2 of...Ch. 15 - Suppose a new mutation arises in a mitochondrial...Ch. 15 - Describe at least two ways in which the...Ch. 15 - Why are severe mitochondrial or chloroplast gene...Ch. 15 - Suppose you are examining a newly found plant...Ch. 15 - A form of male sterility in corn is inherited...Ch. 15 - Plant breeders have long appreciated the...Ch. 15 - A mutant haploid strain of Saccharomyces...Ch. 15 - Prob. 20PCh. 15 - What characteristics in a human pedigree suggest a...Ch. 15 - The first person in the family represented by the...Ch. 15 - In 1988, neurologists in Australia reported the...Ch. 15 - If you were a genetic counselor and had a patient...Ch. 15 - Kearns-Sayre syndrome KSS, Pearson syndrome, and...Ch. 15 - Many clinically relevant mitochondrial diseases...Ch. 15 - Leigh syndrome is characterized by psychomotor...Ch. 15 - All mutations in mitochondrial genes ultimately...Ch. 15 - How could researchers have determined that the...
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
- Leigh syndrome is characterized by psychomotor regression: that is, the progressive loss of mental andmovement abilities. Patients also suffer from lacticacidosis, a condition in which mitochondrial respiration is deficient, so their tissues metabolize glucoseanaerobically, leading to the buildup of lactate. Somepatients with Leigh syndrome have a mutation in themitochondrial gene MT-CO3, which encodes a subunit of the electron transport complex cytochromec oxidase. Other patients diagnosed with Leigh syndrome have a loss-of-function mutation in the nucleargene SURF1, which encodes a factor needed for theassembly of this same enzyme complex.a. How can the same symptoms result from mutationsin a mitochondrial gene and from mutations in anuclear gene?arrow_forwardA genetic disease called glucose-6-phosphate dehydrogenase deficiency is inherited in a manner similar to that of sickle-cell anemia except that it occurs most frequently in males. The defective enzyme cannot keep erythrocytes supplied with sufficient amounts of the antioxidant molecule NADPH NADPH protects cell membranes and other cellular structures from oxidation. Describe in general terms the inheritance pattern of this molecular disease. Why do you think that the antimalarial drug primaquine, which stimulates peroxide formation, results in devastating cases of hemolytic anemia in carriers of the defective gene? Does it surprise you that this genetic anomaly is commonly found in African and Mediterranean populations?arrow_forwardHere we utilize a novel, well-characterized, endogenous mitochondrial mutation in the ATP6 gene of Drosophila melanogaster with a nearly complete loss of ATP synthase activity. These Drosophila mutants have a missense mutation in ATP6 (G to A transition resulting in a glycine to glutamate change at position 116 in the protein), the mitochondrial gene encoding subunit 6 of the F1Fo-ATP synthase(complex V of the respiratory chain. ATP6 allows for the hydrogen ion translocation required for the rotation of the Fo motor and the production of ATP from ADP. Drosophila ATP61 mutants model human mitochondrial encephalomyopathy and demonstrate phenotypes associated with degenerative disease, including: reduced longevity, mitochondrial pathology, progressive neural dysfunction, tissue degeneration and locomotor impairment. ATP61 Drosophila mutants exhibit a stereotyped phenotypic progression that is analogous to the symptomatic progression reported for many human mitochondrial disease…arrow_forward
- The DNA located inside of mitochondria exhibits approximately ten times the mutation rate seen in nuclear DNA. Provide an explanation as to why this is the case and what are the effects of this higher mutation rate of mitochondrial DNA on disease processes?arrow_forwardYarrowia lipolytica(Yl) is a non-conventional yeast that diverged from baker’s yeast, Saccharomyces cerevisiae(Sc), early in evolutionary history. The regulation of glycolytic enzymes in Yl differs from that of Sc. The data below pertain to regulation of phosphofructokinase 1 (PFK). Data for Yl is shown with black circles and data for Sc is shown with white circles. Pfk for both species is a homo-octomer (eight identical subunits). Given the data below, which species is more likely to be susceptible to allosteric modification? Briefly explain.arrow_forwardWhy does it make good physiological sense that regular bouts of prolonged exercise will result in mitochondrial biogenesis?arrow_forward
- Pompe disease is due to a deficiency in lysosomal α-1,4-glucosidase, also called acid maltase. Lysosomes function as recycling centers in the cell and normally degrade excess muscle glycogen into glucose for the energy-converting reactions of the glycolytic pathway. Pompe disease was described in 1932 by Dutch pathologist Johann Pompe, who recognized that lysosomes in the affected patient's accumulated large amounts of glycogen. However, Henri Hers—the same Belgian pathologist who described the symptoms of liver glycogen phosphorylase deficiency (Hers disease)—discovered in 1965 that Pompe disease was due to a lysosomal α-1,4-glucosidase deficiency. Enzyme deficiency Disease name Organ Disease symptoms Lysosomal α-1,4- glucosidase Pompe All organs Heart failure in infantile form; muscle defects in juvenile form Answer these questions: What protein/enzyme does the mutation effects? Symptoms and, if you can, how are the symptoms…arrow_forwardThrough your biotechnology research project at the Tiger One Brewery, you engineered a glucose transporter in a yeast strain in order to increase its rate of fermentation. Your colleague recorded the glucose uptake data shown below from the yeast strain you developed and to your surprise, you found out that your engineered glucose transporter has three- fold more affinity to glucose compared to the wild-type (native/unmodified) glucose transporter. From the figure below, can you predict the Km of the wild-type glucose transporter? Note: The Vmax of the wildtype and engineered transporters are the same in the experimental setup, and the plot below is the data of your engineered glucose transporter and NOT the wildtype (native/unmodified) transporter. Glucose uptake 100.. 50- 25arrow_forwardYeast cells are eukaryotes, and they require a functional secretory pathway to grow and to maintain cellular organization. But surprisingly, when SRP is removed from yeast cells by deleting the relevant genes, the cells are still alive (although they grow slowly). a) How can yeast survive without SRP? Propose two alternative hypotheses. b) How might electron microscopy of normal and SRP-deficient yeast cells help you to distinguish between these two hypotheses?arrow_forward
- Leber’s Hereditary Optic Neuropathy (LHON) is a disease that involves degeneration of neural cells in the retina and results in loss of central vision. The disease is caused by mutations in any one of three genes in the mitochondrial genome that encode proteins involved in oxidative phosphorylation. In a genetic counseling clinic, a woman and her husband seek advice on the potential that any of their children would be afflicted with LHON. The husband's mother and father, both exhibit symptoms of the disease, but the woman does not. What is a reasonable advising statement to make? a. The couple should be advised that all of their children are likely to display symptoms of LHON. b. There is not enough information to advise this couple. c. The couple should be advised that none of their children will be affected. d. The couple should be advised that all their male children will display symptoms of LHON, but female children will be unaffected. e. The couple should be…arrow_forwardLeber's Hereditary Optic Neuropathy (LHON) is a disease that involves degeneration of neural cells in the retina and results in loss of central vision. The disease is caused by mutations in any one of three genes in the mitochondrial genome that encode proteins involved in oxidative phosphorylation. In a genetic counseling clinic, a woman and her husband seek advice on the potential that any of their children would be afflicted with LHON. The husband's mother and father, both exhibit symptoms of the disease, but the woman does not. What is a reasonable advising statement to make? There is not enough information to advise this couple. a. The couple should be advised that all of their children are likely to display symptoms of LHON. b. The couple should be advised that all their female children will display symptoms of LHON, but male children will be unaffected. C. The couple should be advised that all their male children will display symptoms of LHON, but female children will be…arrow_forwardLeber’s Hereditary Optic Neuropathy (LHON) is a disease that involves degeneration of neural cells in the retina and results in loss of central vision. The disease is caused by mutations in any one of three genes in the mitochondrial genome that encode proteins involved in oxidative phosphorylation. In a genetic counseling clinic, a woman and her husband seek advice on the potential that any of their children would be afflicted with LHON. The husband's mother and father, both exhibit symptoms of the disease, but the woman does not. What is a reasonable advising statement to make?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:PEARSONBiology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStaxAnatomy & 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 & CompanyLaboratory 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
Mitochondrial mutations; Author: Useful Genetics;https://www.youtube.com/watch?v=GvgXe-3RJeU;License: CC-BY