Table of contents

1. Introduction to Genetics51m
2. Mendel's Laws of Inheritance3h 37m
3. Extensions to Mendelian Inheritance2h 41m
4. Genetic Mapping and Linkage2h 28m
5. Genetics of Bacteria and Viruses1h 21m
6. Chromosomal Variation1h 48m
7. DNA and Chromosome Structure56m
8. DNA Replication1h 10m
9. Mitosis and Meiosis1h 34m
10. Transcription1h 0m
11. Translation58m
12. Gene Regulation in Prokaryotes1h 19m
13. Gene Regulation in Eukaryotes44m
14. Genetic Control of Development44m
15. Genomes and Genomics1h 50m
16. Transposable Elements47m
17. Mutation, Repair, and Recombination1h 6m
18. Molecular Genetic Tools19m
- Genetic Cloning
  9m
- Methods for Analyzing DNA
  9m
19. Cancer Genetics29m
- Overview of Cancer
  21m
- Cancer Mutations
  7m
20. Quantitative Genetics1h 26m
21. Population Genetics50m
- Hardy Weinberg
  19m
- Allelic Frequency Changes
  31m
22. Evolutionary Genetics29m

3. Extensions to Mendelian Inheritance

Organelle DNA

Genetics

3. Extensions to Mendelian Inheritance

Organelle DNA

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2:26 minutes

Problem 20

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?

Verified step by step guidance

Understand the concept of heteroplasmy: Heteroplasmy refers to the presence of more than one type of mitochondrial DNA (mtDNA) within a single cell. This can result from mutations in mtDNA, leading to a mixture of normal and mutated mtDNA molecules.

Recognize the role of mitochondrial replication and segregation: Mitochondria replicate independently of the cell cycle, and their DNA is randomly distributed during cell division. This random segregation can lead to variability in the proportion of mutated and normal mtDNA in different cells.

Consider the impact of mtDNA mutations: Mutations in mtDNA can arise due to errors in replication or damage from reactive oxygen species. These mutations can accumulate over time, contributing to the heteroplasmic pool.

Acknowledge the bottleneck effect: During the development of oocytes (egg cells), a small subset of mitochondria is selected to populate the next generation. This bottleneck effect can amplify or reduce the proportion of mutated mtDNA, leading to variability in heteroplasmy levels.

Factor in selective pressures: Certain mutations in mtDNA may confer a selective advantage or disadvantage to mitochondria, influencing their replication and survival. This can further contribute to the variability in the mitochondrial pool within a cell or individual.

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Key Concepts

Here are the essential concepts you must grasp in order to answer the question correctly.

Heteroplasmy

Heteroplasmy refers to the presence of more than one type of mitochondrial DNA (mtDNA) within a single cell or individual. This condition can arise from mutations in mtDNA, leading to a mixture of normal and mutated genomes. The level of heteroplasmy can vary among tissues and individuals, influencing mitochondrial function and health.

Mitochondrial DNA (mtDNA)

Mitochondrial DNA is the genetic material found in mitochondria, the energy-producing organelles in cells. Unlike nuclear DNA, mtDNA is inherited maternally and is circular in structure. Variations in mtDNA can affect cellular energy production and are linked to various genetic disorders, making its study crucial in understanding mitochondrial function and disease.

Mitochondrial Dynamics

Mitochondrial dynamics encompass the processes of mitochondrial fusion and fission, which regulate the shape, size, and number of mitochondria within a cell. These processes are essential for maintaining mitochondrial function, quality control, and distribution during cell division. Variations in these dynamics can lead to a heterogeneous population of mitochondria, contributing to the observed heteroplasmy.

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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

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

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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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?

Key Concepts

Heteroplasmy

Mitochondrial DNA (mtDNA)

Mitochondrial Dynamics

Watch next

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?