A male mouse from a true-breeding strain of hyperactive animals is crossed with a female mouse from a true-breeding strain of lethargic animals. (These are both hypothetical strains.) All the progeny are lethargic. In the F₂ generation, all offspring are lethargic. What is the best genetic explanation for these observations? Propose a cross to test your explanation.

Earlier, we described CC, the cat created by nuclear transfer cloning, whereby a diploid nucleus from one cell is injected into an enucleated egg cell to create an embryo. Cattle, sheep, rats, dogs, and several other species have been cloned using nuclei from somatic cells. Embryos and adults produced by this approach often show a number of different mitochondrial defects. Explain possible reasons for the prevalence of mitochondrial defects in embryos created by nuclear transfer cloning.
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Key Concepts
Nuclear Transfer Cloning
Mitochondrial DNA Inheritance
Somatic Cell Nuclear Transfer (SCNT) Defects
Consider the case where a mutation occurs that disrupts translation in a single human mitochondrion found in the oocyte participating in fertilization. What is the likely impact of this mutation on the offspring arising from this oocyte?
What is the endosymbiotic theory, and why is this theory relevant to the study of extranuclear DNA in eukaryotic organelles?
Mitochondrial replacement therapy (MRT) offers a potential solution for women with mtDNA-based diseases to have healthy children. Based on what you know about the importance of nuclear gene products to mitochondrial functions, will MRT ensure that children will not inherit or develop a mtDNA-based diseases?
The specification of the anterior–posterior axis in Drosophila embryos is initially controlled by various gene products that are synthesized and stored in the mature egg following oogenesis. Mutations in these genes result in abnormalities of the axis during embryogenesis. These mutations illustrate maternal effect. How do such mutations vary from those produced by organelle heredity? Devise a set of parallel crosses and expected outcomes involving mutant genes that contrast maternal effect and organelle heredity.
The maternal-effect mutation bicoid (bcd) is recessive. In the absence of the bicoid protein product, embryogenesis is not completed. Consider a cross between a female heterozygous for the bicoid alleles (bcd⁺/bcd⁻) and a male homozygous for the mutation (bcd⁻/bcd⁻).
Predict the outcome (normal vs. failed embryogenesis) in the F₁ and F₂ generations of the cross described.
