ND STONY BROOK UNIVERSITY LOOSELEAF GENETICS: FROM GENES TO GENOMES
6th Edition
ISBN: 9781260406092
Author: HARTWELL, Leland, HOOD, Leroy, Goldberg, Michael
Publisher: Mcgraw-hill Education/stony Brook University
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Textbook Question
Chapter 15, Problem 28P
All mutations in mitochondrial genes ultimately affect (whether directly or indirectly) the key function of mitochondria, which is to make ATP. Why then do mutations in different genes cause different diseases, with specific symptoms? (Note: The answer to this question is not known, but your speculations will help you think about the material in this chapter.)
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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?
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…
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?
Most diseases are caused by disruptions in cellular function.
You are to research a disease that is a disturbance at the cellular level. Usually, there are problems with the organelles within the cells. So essentially, you can look up things like....mitochondrial diseaselysosomal disorderscellular receptor disorders
Once you have found a disease you should include the following in your 2 paragraph summary.1-Description and how is occurs2-Is it genetic?3-Are there cures?4-What does research show as far as cures or treatments?5-How does it affect one's life?
Chapter 15 Solutions
ND STONY BROOK UNIVERSITY LOOSELEAF 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...
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- All mutations in mitochondrial genes ultimately affect (whether directly or indirectly) the key function of mitochondria, which is to make ATP. Why then do mutations in different genes cause different diseases, with specific symptoms?arrow_forwardThe 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_forwardAcatalasemia is a rare autosomal recessive condition that results in no expression of the enzyme catalase; however, persons with this condition are usually only mildly affected. The enzyme catalase is found in most organisms and is a protection against oxidative damage, specifically breaking down the highly reactive oxygen species, hydrogen peroxide. Symptoms may include mouth ulcers that disappear with good dental hygiene; with poor dental hygiene, the ulcers can lead to gangrene in the mouth soft tissues. Persons with this condition usually do not know they are affected unless a family member is tested for the mutation. Dejah recently learned that her Uncle Malik had a dental surgery that was complicated by mouth ulcers and gangrenous tissue that had to be removed. The oral surgeon had learned about genetic conditions that affect oral hygiene and recognized that this could be acatalasemia, and ordered genetic testing. Uncle Malik was positive for this recessive condition, having…arrow_forward
- Familial hypercholesterolemia is a genetic condition characterized by an absence of functional LDL receptors on the surface of cells. Patients who are homozygous for familial hypercholesterolemia usually die of coronary artery disease in childhood. Which of the following disorders could mimic the symptoms of familial hypercholesterolemia? (A) LDL receptor endocytosis machinery is non-functional (B) lack of ATP allosteric site on AMPK(C) Golgi proteases that cleave SREBP are not synthesized (D) mutation in the HMG CoA reductase SRE sequence. (E) inability to secrete VLDL from the liverarrow_forwardThe biogenesis of functional mitochondria is dependent upon the products of both nuclear and mitochondrial genes, which poses several regulatory and logistical issues. Interestingly, many of the nuclear genes encoding mitochondrial proteins are regulated at the transcriptional level by Myc (activates transcription) and p53 (often represses transcription). Does this make sense? Why or why not?arrow_forwardSome living organisms are under considerable pressure tostreamline their genomes for the sake of more efficientoperation. As a result, the mitochondria of eukaryotic species have lost, to one degree or another, the overwhelmingmajority of their genes. During this process, several hundred mitochondrial genes were transferred to the nucleargenome. Yet mitochondria still retain a genome with thecapacity to produce several electron transport proteins.Review mitochondrial electron transport and suggest areason why these energy-generating organelles retained thegenes to produce this set of molecules.arrow_forward
- Here 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_forwardGalactosemia is a metabolic disorder characterized by the inability to metabolize the sugar galactose. People with galactosemia suffer from liver, kidney, and brain damage among other symptoms. A gene mutation underlying galactosemia was identified by sequencing the genome of a person with galactosemia. What additional evidence would support the hypothesis that the mutation in the candidate gene causes the disease?arrow_forwardYou are studying the M-cyclin. You treat mitotic cells with an inhibitor of the proteasome and find that M-cyclin is no longer degraded and that this prolongs mitosis. You also find that in the presence of the inhibitor, M-cyclin is now running slower/larger in a Western than you have previously observed. In 1-2 sentences, explain why this might be happening. Edit View Insert Format Tools Table 12pt Paragraph B IU Αν S A C I AT²✓ #tv A MacBook Air X : Garrow_forward
- 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…arrow_forwardA 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.arrow_forwardnvestigate references dealing with the technical and ethical challenges surrounding mitochondrial replacement therapy (MRT). Consider the following questions: Differentiate between MRT methods: pronuclear transfer (PNT) versus maternal spindle transfer (MST). Much of the controversy surrounding MRT methods has been triggered by the phrase “three-parent babies” in media headlines. Do you think that this phrase is an accurate description of children born following mitochondrial replacement? Summarize the ethical arguments used to support and oppose the use of MRT in humans. In your opinion, which arguments have validity, and whyarrow_forward
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