3. Extensions to Mendelian Inheritance

Organelle DNA

3. Extensions to Mendelian Inheritance

Organelle DNA

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Problem 17Sanders - 3rd Edition

Textbook Question

The first person in a family to exhibit Leber hereditary optic neuropathy (LHON) was II-3 in the pedigree shown below, and all of her children also exhibited the disease. Provide two possible explanations as to why II-3's mother (I-1) did not exhibit symptoms of LHON.

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Identify that Leber hereditary optic neuropathy (LHON) is a mitochondrial disorder, which means it is passed through the maternal line.

Observe that individual II-3 is affected and all her children (III-1, III-2, III-3) are also affected, indicating maternal inheritance.

Consider that I-1, the mother of II-3, might not exhibit symptoms due to heteroplasmy, where a mixture of normal and mutated mitochondria exists, and the proportion of mutated mitochondria is not sufficient to cause symptoms.

Another possibility is that I-1 has a lower penetrance of the disease, meaning she carries the mutation but does not express the symptoms due to other genetic or environmental factors.

Conclude that the absence of symptoms in I-1 does not preclude her from being a carrier of the mitochondrial mutation responsible for LHON.

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Textbook Question

In this chapter, we focused on extranuclear inheritance and how traits can be determined by genetic information contained in mitochondria and chloroplasts, and we discussed how expression of maternal genotypes can affect the phenotype of an organism. At the same time, we found many opportunities to consider the methods and reasoning by which much of this information was acquired. From the explanations given in the chapter, what answers would you propose to the following fundamental questions?

What observations support the endosymbiotic theory?

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Textbook Question

In this chapter, we focused on extranuclear inheritance and how traits can be determined by genetic information contained in mitochondria and chloroplasts, and we discussed how expression of maternal genotypes can affect the phenotype of an organism. At the same time, we found many opportunities to consider the methods and reasoning by which much of this information was acquired. From the explanations given in the chapter, what answers would you propose to the following fundamental questions?

How did the discovery of three categories of petite mutations in yeast lead researchers to postulate extranuclear inheritance of colony size?

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Textbook Question

How are some of the characteristics of the organelles (the mitochondria and chloroplasts) explained by their origin as ancient bacterial endosymbionts?

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Textbook Question

Streptomycin resistance in Chlamydomonas may result from a mutation in either a chloroplast gene or a nuclear gene. What phenotypic results would occur in a cross between a member of an mt⁺ strain resistant in both genes and a member of a strain sensitive to the antibiotic? What results would occur in the reciprocal cross?

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Textbook Question

What is the evidence that transfer of DNA from the organelles to the nucleus continues to occur?

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Textbook Question

Draw a graph depicting the relative amounts of nuclear DNA present in the different stages of the cell cycle (G₁,S,G₂,M). On the same graph, plot the amount of mitochondrial DNA present at each stage of the cell cycle.

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Textbook Question

What is the evidence that the ancient mitochondrial and chloroplast endosymbionts are related to the alphaproteobacteria and cyanobacteria, respectively?

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Textbook Question

Outline the steps required for a gene originally present in the endosymbiont genome to be transferred to the nuclear genome and be expressed, and for its product to be targeted back to the organelle of origin.

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Textbook Question

Consider the phylogenetic tree presented in Figure 17.17. How were the origins of secondary endosymbiosis in the brown algae determined?

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Textbook Question

You are a genetic counselor, and several members of the family whose pedigree for an inherited disorder is depicted in Genetic Analysis 17.2 consult with you about the probability that their progeny may be afflicted. What advice would you give individuals III-1, III-2, III-4, III-6, III-8, and III-9?

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Textbook Question

A mutation in Arabidopsis immutans results in the necrosis (death) of tissues in a mosaic configuration. Examination of the mitochondrial DNA detects deletions of various regions of the mitochondrial genome in the tissues that are necrotic. When immutans plants are crossed with wild-type plants, the are wild type, and the are wild type and immutans in a 3:1 ratio. Explain the inheritance of the immutans mutation and a possible origin of the mitochondrial DNA deletions.

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Textbook Question

What type or types of inheritance are consistent with the following pedigree?

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Textbook Question

What is the endosymbiotic theory, and why is this theory relevant to the study of extranuclear DNA in eukaryotic organelles?

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Textbook Question

A 50-year-old man has been diagnosed with MELAS syndrome (see Figure 17.6). His wife is phenotypically normal, and there is no history of MELAS syndrome in either of their families. The couple is concerned about whether their children will develop the disease. As a genetic counselor, what will you tell them? Would your answer change if it were the mother who exhibited disease symptoms rather than the father?

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Textbook Question

Mutations in mitochondrial DNA appear to be responsible for a number of neurological disorders, including myoclonic epilepsy and ragged-red fiber disease, Leber's hereditary optic neuropathy, and Kearns-Sayre syndrome. In each case, the disease phenotype is expressed when the ratio of mutant to wild-type mitochondria exceeds a threshold peculiar to each disease, but usually in the 60 to 95 percent range.

Compared with the vast number of mitochondria in an embryo, the number of mitochondria in an ovum is relatively small. Might such an ooplasmic mitochondrial bottleneck present an opportunity for therapy or cure? Explain.

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Textbook Question

Mutations in mitochondrial DNA appear to be responsible for a number of neurological disorders, including myoclonic epilepsy and ragged-red fiber disease, Leber's hereditary optic neuropathy, and Kearns-Sayre syndrome. In each case, the disease phenotype is expressed when the ratio of mutant to wild-type mitochondria exceeds a threshold peculiar to each disease, but usually in the 60 to 95 percent range.

Given that these are debilitating conditions, why has no cure been developed? Can you suggest a general approach that might be used to treat, or perhaps even cure, these disorders?

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Textbook Question

In 1918, the Russian tsar Nicholas II was deposed, and he and his family were reportedly executed and buried in a shallow grave. During this chaotic time, rumors abounded that the youngest daughter, Anastasia, had escaped. In 1920, a woman in Germany claimed to be Anastasia. In 1979, remains were recovered for the tsar, his wife (the Tsarina Alexandra), and three of their children, but not Anastasia. How would you evaluate the claim of the woman in Germany?

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Textbook Question

Payne, B. A. et al. (2013) present evidence that a low level of heteroplasmic mtDNA exists in all tested healthy individuals.

What are two likely sources of such heteroplasmy?

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Textbook Question

Payne, B. A. et al. (2013) present evidence that a low level of heteroplasmic mtDNA exists in all tested healthy individuals.

What genetic conditions within a given mitochondrion are likely to contribute to such a variable pool of mitochondria?

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Textbook Question

The dodo bird (Raphus cucullatus) lived on the Mauritius Islands until the arrival of European sailors, who quickly hunted the large, placid, flightless bird to extinction. Rapid morphological evolution such as often accompanies island isolation had caused the bird's huge size and obscured its physical resemblance to any near relatives. However, sequencing of mitochondrial DNA from dodo bones reveals that they were pigeons, closely related to the Nicobar pigeon from other islands in the Indian Ocean. Why was mitochondrial DNA suited to the study of this extinct species?

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Textbook Question

As mentioned in Section 9.3, mtDNA accumulates mutations at a rate approximately ten times faster than nuclear DNA. Thus geneticists can use mtDNA variations as a 'molecular clock' to study genetic variation and the movement of ancestral human populations from Africa to different areas of the world more than 125,000 years ago. Propose an explanation for how an analysis of mtDNA can be used to construct family trees of human evolution.

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Textbook Question

Because offspring inherit the mitochondrial genome only from the mother, evolutionarily the mitochondrial genome in males encounters a dead end. The mitochondrial genome in males has no significant impact on the genetic information of future generations. Scientists have proposed that this can result in an accumulation of mutations that have a negative impact on genetic fitness of males but not females. Experiments with Drosophila support this possibility. What experimental data or evidence would you want to evaluate or consider to determine if an accumulation of mtDNA mutations negatively impacts the fitness of males of any species?

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Textbook Question

As described in this chapter, mothers will pass on a mitochondrial defect to their offspring. In a type of gene therapy, one approach to circumvent this problem is to have two different maternal contributions, with the nucleus of the female with the defective mitochondria being placed in an enucleated egg derived from a female with normal mitochondria. After fertilization, the resulting offspring would have three parental sources of DNA—with nuclear DNA derived from a mother and a father, and mitochondrial DNA derived from another 'mother.' Recently, children with this genetic makeup have been born, but the elimination of defective mitochondria is not complete, with the amount of defective mitochondria derived from the defective mother ranging from 0 to 9%. Discuss potential complications resulting from such a mixture of genomes.

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