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A female mouse of genotype MITO-/- carries a mutation in an important regulator of mitochondrial function. The phenotype of the mouse is notable for poor CNS development, severely reduced exercise capacity and early heart failure.

In a second experiment, healthy mitochondria were directly injected into the affected cells with subsequent cellular analysis showing improvement in mitochondrial function.

To see if the phenotype could be rescued in vivo, the affected female was crossed with an unaffected male of genotype MITO+/+.

What number of the offspring will have the SAME phenotype as their mother?


0% as the father’s mitochondria will rescue the phenotype.


100% as the father’s mitochondria and mitochondrial DNA will not affect the progeny.


75% as the mutation is dominant.


25% as the mutation is recessive.

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